35.6: Nervous System Disorders - Biology

35.6: Nervous System Disorders - Biology

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  • 35.6A: Neurodegenerative Disorders
    Alzheimer’s disease and Parkinson’s disease are both neurodegenerative disorders characterized by loss of nervous system functioning.
  • 35.6B: Neurodevelopmental Disorders - Autism and ADHD
    Autism and ADHD are neurodevelopmental disorders that arise when nervous system development is disrupted. Neurodevelopmental disorders occur when the development of the nervous system is disturbed. There are several different classes of neurodevelopmental disorders. Some, like Down Syndrome, cause intellectual deficits, while others specifically affect communication, learning, or the motor system. Some disorders, such as autism spectrum disorder and ADHD disorder, have complex symptoms.
  • 35.6C: Neurodevelopmental Disorders - Mental Illnesses
    Schizophrenia and depression are just two examples of mental illnesses caused by a disorder of the nervous system.
  • 35.6D: Other Neurological Disorders
    Epilepsy and stroke are examples of neurological disorders that arise from malfunctions in the nervous system.

Overview of the qualifiers for the list.

Other Qualifiers
A "Accepted" in prior version of this table.
C A disease, regarded as autoimmune, that is often found in individuals with another autoimmune condition. This designation is given to diseases that are classified by Rose and Bona as having "circumstantial" evidence of autoimmune etiology. Diseases in this list with a "C" are, therefore, actual autoimmune diseases, rather than comorbid symptoms, which appear after this list.
E Disease is an autoimmune response triggered by a specific environmental factor.
F Disease is only caused by autoimmunity in only a fraction of those who suffer from it.
I Described as an autoinflammatory disease.
L Evidence to indicate autoimmunity is extremely limited or circumstantial.
M Disease appears under Autoimmune Diseases in MeSH.
N Not listed in prior version of this table.
R Disease appeared in prior version but has been renamed. In renaming, precedence has been given to scientific names over those based on discoverers.
S "Suspected" in the prior version of this table.
T Disease has a known trigger, such as viral infection, vaccination, or injury.
X An extremely rare disease, which would suggest limited opportunity to study it and conclusively determine whether it is caused by autoimmunity.
Y Listed in the prior version of this table with "Accepted/Suspected" left blank.

Major organs Edit

Level of acceptance for autoimmunity Hypersensitivity

Glands Edit

Level of acceptance for autoimmunity Hypersensitivity

Digestive system Edit

Level of Acceptance for Autoimmunity Hypersensitivity

Tissue Edit

Level of acceptance for autoimmunity Hypersensitivity

This list includes conditions that are not diseases but signs common to autoimmune disease. Some, such as chronic fatigue syndrome, are controversial. [2] These conditions are included here because they are frequently listed as autoimmune diseases but should not be included in the list above until there is more consistent evidence.

Level of Acceptance for Autoimmunity Hypersensitivity

At this time, there is not sufficient evidence—direct, indirect, or circumstantial—to indicate that these diseases are caused by autoimmunity. These conditions are included here because:

Tumor Biology of Childhood CNS Atypical Teratoid/Rhabdoid Tumor

Childhood central nervous system (CNS) atypical teratoid/rhabdoid tumor (AT/RT) was first described as a discrete clinical entity in 1987 [1] on the basis of its distinctive pathologic and genetic characteristics. Before then, it was most often classified as a medulloblastoma, CNS primitive neuroectodermal tumor (CNS PNET), or choroid plexus carcinoma. The World Health Organization (WHO) classifies AT/RT as an embryonal grade IV neoplasm.[2]

Histologically, AT/RT is morphologically heterogeneous, typically containing sheets of large epithelioid cells with abundant eosinophilic cytoplasm and scattered rhabdoid cells, most often with accompanying components of primitive neuroectodermal cells (small round blue cells), mesenchymal cells, and/or glial cells.[3]

Immunohistochemical staining for epithelial markers (cytokeratin or epithelial membrane antigen), glial fibrillary acidic protein, synaptophysin (or neurofilament), and smooth muscle (desmin) may help to identify the heterogeneity of differentiation, but will vary depending on the cellular composition.[4] Rhabdoid cells, while not present in all AT/RTs, will express vimentin, epithelial membrane antigen, and smooth muscle actin.

Immunohistochemistry for the SMARCB1 protein is useful in establishing the diagnosis of AT/RT. A loss of SMARCB1 staining is noted in neoplastic cells, but staining is retained in non-neoplastic cells (e.g., vascular endothelial cells).[5-7]

AT/RT is a rapidly growing tumor that can have an MIB-1 labeling index of 50% to 100%.[8]

Genomics of CNS Atypical Teratoid/Rhabdoid Tumor (AT/RT)

SMARCB1 and SMARCA4 genes

AT/RT was the first primary pediatric brain tumor in which a candidate tumor suppressor gene, SMARCB1 (previously known as INI1 and hSNF5), was identified.[9] SMARCB1 is genomically altered in most rhabdoid tumors, including CNS, renal, and extrarenal rhabdoid malignancies.[9] SMARCB1 is a component of a SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin-remodeling complex.[10]

Rare cases of rhabdoid tumors expressing SMARCB1 and lacking SMARCB1 mutations have also been associated with somatic or germline mutations of SMARCA4/BRG1, another member of the SWI/SNF chromatin-remodeling complex.[7,11,12]

Less commonly, SMARCA4-negative (with retained SMARCB1) tumors have been described.[7,11,12] Loss of SMARCB1 or SMARCA4 staining is a defining marker for AT/RT.

The 2016 WHO classification defines AT/RT by the presence of either SMARCB1 or SMARCA4 alterations. Tumors with histological features of AT/RT that lack these genomic alterations are termed CNS embryonal tumor with rhabdoid features.[2]

Despite the absence of recurring genomic alterations beyond SMARCB1 and SMARCA4,[13-15] biologically distinctive subsets of AT/RT have been identified.[16,17] The following three distinctive subsets of AT/RT were identified through the use of DNA methylation arrays for 150 AT/RT tumors and gene expression arrays for 67 AT/RT tumors:[17]

  • AT/RT TYR: This subset represented approximately one-third of cases and was characterized by elevated expression of melanosomal markers such as TYR (the gene encoding tyrosinase). Cases in this subset were primarily infratentorial, with most presenting in children aged 0 to 1 year and showing chromosome 22q loss.[17] For patients with AT/RT TYR, the mean overall survival (OS) was 37 months in a clinically heterogeneous group (95% confidence interval [CI], 18󈞤 months).[18] In the prospective European Rhabdoid Registry (EU-RHAB) series, patients aged 1 year and older with an AT/RT-TYR subgroup designation demonstrated a 5-year OS rate of 71%, while those younger than 1 year with a non-TYR subgroup designation had a very poor survival rate.[19]
  • AT/RT SHH: This subset represented approximately 40% of cases and was characterized by elevated expression of genes in the sonic hedgehog (SHH) pathway (e.g., GLI2 and MYCN). Cases in this subset occurred with similar frequency in the supratentorium and infratentorium. While most patients presented before the age of 2 years, approximately one-third of patients presented between the ages of 2 and 5 years.[17] For patients with AT/RT SHH, the mean OS was 16 months (95% CI, 8󈞅 months).[18]
  • AT/RT MYC: This subset represented approximately one-fourth of cases and was characterized by elevated expression of MYC. AT/RT MYC cases tended to occur in the supratentorial compartment. While most AT/RT MYC cases occurred by the age of 5 years, AT/RT MYC represented the most common subset diagnosed at age 6 years and older. Focal deletions of SMARCB1 were the most common mechanism of SMARCB1 loss for this subset.[17] For patients with AT/RT MYC, the mean OS was 13 months (95% CI, 5󈞂 months).[18]

Cribriform neuroepithelial tumor is a brain cancer that also presents in young children and has genomic and epigenomic characteristics that are very similar to AT/RT TYR.[18] (Refer to the Cribriform Neuroepithelial Tumor section of the PDQ summary on Childhood Central Nervous System Atypical Teratoid/Rhabdoid Tumor Treatment for more information.)

In addition to somatic mutations, germline mutations in SMARCB1 have been reported in a substantial subset of patients with AT/RT.[9,20] A study of 65 children with rhabdoid tumors found that 23 (35%) had germline mutations and/or deletions of SMARCB1.[5] Children with germline alterations in SMARCB1 presented at an earlier age than did sporadic cases (median age, approximately 5 months vs. 18 months) and were more likely to present with synchronous, multifocal tumors.[5] One parent was found to be a carrier of the SMARCB1 germline abnormality in 7 of 22 evaluated cases showing germline alterations, with four of the carrier parents being unaffected by SMARCB1-associated cancers.[5] This indicates that AT/RT shows an autosomal dominant inheritance pattern with incomplete penetrance.

Gonadal mosaicism has also been observed, as evidenced by families in which multiple siblings are affected by AT/RT and have identical SMARCB1 alterations, but both parents lack a SMARCB1 mutation/deletion.[5,6] Screening for germline SMARCB1 mutations in children diagnosed with AT/RT is suggested for counseling families on the genetic implications of their child’s AT/RT diagnosis.[5] Preliminary recommendations for the genetic evaluation and subsequent presymptomatic screening of nonaffected mutation carriers (including parents and siblings of affected patients) have been reported and are likely to evolve as the understanding of rhabdoid tumor predisposition improves.[21] In patients with a predisposition to AT/RT, whole-body MRI may help to identify synchronous rhabdoid tumors outside of the CNS.

Loss of SMARCB1 or SMARCA4 protein expression has therapeutic significance, because this loss creates a dependence of the cancer cells on EZH2 activity.[22] Preclinical studies have shown that some AT/RT xenograft lines with SMARCB1 loss respond to EZH2 inhibitors with tumor growth inhibition and occasional tumor regression.[23,24] In a study of the EZH2 inhibitor tazemetostat, objective responses were observed in adult patients whose tumors had either SMARCB1 or SMARCA4 loss (non-CNS malignant rhabdoid tumors and epithelioid sarcoma).[25] (Refer to the Treatment of Recurrent Childhood CNS Atypical Teratoid/Rhabdoid Tumor section of this summary for more information.)

Rhabdoid Tumor Predisposition Syndrome (RTPS)

RTPS, which is primarily related to germline SMARCB1 alterations (and less commonly to germline SMARCA4 alterations), has been clearly defined.[9,20] RTPS is highly suggested in patients with synchronous occurrence of extracranial malignant rhabdoid tumor (kidney or soft tissue) and AT/RT, bilateral malignant rhabdoid tumors of the kidney, or malignant rhabdoid tumors in two or more siblings.

This syndrome is manifested by a marked predisposition to the development of malignant rhabdoid tumors in infancy and early childhood. Up to one-third of AT/RTs are thought to arise in the setting of RTPS, and most of these occur within the first year of life. The most common non-CNS malignancy of RTPS is malignant rhabdoid tumor of the kidney, which is also noted in infancy.

Cribriform Neuroepithelial Tumor

Cribriform neuroepithelial tumor is histologically and clinically distinct from AT/RT, but it has genomic and epigenomic characteristics that are very similar to AT/RT TYR.[18] Like AT/RT, cribriform neuroepithelial tumor occurs in young children (median age, 1𔃀 years) and tumor cells lack SMARCB1 expression. Histologically, cribriform neuroepithelial tumor is characterized by the presence of cribriform strands and ribbons, but there is an absence of rhabdoid tumor cells with abundant eosinophilic cytoplasm. Like AT/RT TYR, tyrosinase expression is commonly observed. The outcome of patients with cribriform neuroepithelial tumor is more favorable than the outcome of patients with AT/RT TYR, with only one death reported among ten children with cribriform neuroepithelial tumor.[18]

  1. Rorke LB, Packer RJ, Biegel JA: Central nervous system atypical teratoid/rhabdoid tumors of infancy and childhood: definition of an entity. J Neurosurg 85 (1): 56-65, 1996. [PUBMED Abstract]
  2. Louis DN, Perry A, Reifenberger G, et al.: The 2016 World Health Organization Classification of Tumors of the Central Nervous System: a summary. Acta Neuropathol 131 (6): 803-20, 2016. [PUBMED Abstract]
  3. Louis DN, Ohgaki H, Wiestler OD: WHO Classification of Tumours of the Central Nervous System. 4th rev.ed. IARC Press, 2016.
  4. McLendon RE, Adekunle A, Rajaram V, et al.: Embryonal central nervous system neoplasms arising in infants and young children: a pediatric brain tumor consortium study. Arch Pathol Lab Med 135 (8): 984-93, 2011. [PUBMED Abstract]
  5. Eaton KW, Tooke LS, Wainwright LM, et al.: Spectrum of SMARCB1/INI1 mutations in familial and sporadic rhabdoid tumors. Pediatr Blood Cancer 56 (1): 7-15, 2011. [PUBMED Abstract]
  6. Bruggers CS, Bleyl SB, Pysher T, et al.: Clinicopathologic comparison of familial versus sporadic atypical teratoid/rhabdoid tumors (AT/RT) of the central nervous system. Pediatr Blood Cancer 56 (7): 1026-31, 2011. [PUBMED Abstract]
  7. Hasselblatt M, Gesk S, Oyen F, et al.: Nonsense mutation and inactivation of SMARCA4 (BRG1) in an atypical teratoid/rhabdoid tumor showing retained SMARCB1 (INI1) expression. Am J Surg Pathol 35 (6): 933-5, 2011. [PUBMED Abstract]
  8. Kleihues P, Louis DN, Scheithauer BW, et al.: The WHO classification of tumors of the nervous system. J Neuropathol Exp Neurol 61 (3): 215-25 discussion 226-9, 2002. [PUBMED Abstract]
  9. Biegel JA, Tan L, Zhang F, et al.: Alterations of the hSNF5/INI1 gene in central nervous system atypical teratoid/rhabdoid tumors and renal and extrarenal rhabdoid tumors. Clin Cancer Res 8 (11): 3461-7, 2002. [PUBMED Abstract]
  10. Biegel JA, Kalpana G, Knudsen ES, et al.: The role of INI1 and the SWI/SNF complex in the development of rhabdoid tumors: meeting summary from the workshop on childhood atypical teratoid/rhabdoid tumors. Cancer Res 62 (1): 323-8, 2002. [PUBMED Abstract]
  11. Schneppenheim R, Frühwald MC, Gesk S, et al.: Germline nonsense mutation and somatic inactivation of SMARCA4/BRG1 in a family with rhabdoid tumor predisposition syndrome. Am J Hum Genet 86 (2): 279-84, 2010. [PUBMED Abstract]
  12. Hasselblatt M, Nagel I, Oyen F, et al.: SMARCA4-mutated atypical teratoid/rhabdoid tumors are associated with inherited germline alterations and poor prognosis. Acta Neuropathol 128 (3): 453-6, 2014. [PUBMED Abstract]
  13. Lee RS, Stewart C, Carter SL, et al.: A remarkably simple genome underlies highly malignant pediatric rhabdoid cancers. J Clin Invest 122 (8): 2983-8, 2012. [PUBMED Abstract]
  14. Kieran MW, Roberts CW, Chi SN, et al.: Absence of oncogenic canonical pathway mutations in aggressive pediatric rhabdoid tumors. Pediatr Blood Cancer 59 (7): 1155-7, 2012. [PUBMED Abstract]
  15. Hasselblatt M, Isken S, Linge A, et al.: High-resolution genomic analysis suggests the absence of recurrent genomic alterations other than SMARCB1 aberrations in atypical teratoid/rhabdoid tumors. Genes Chromosomes Cancer 52 (2): 185-90, 2013. [PUBMED Abstract]
  16. Torchia J, Picard D, Lafay-Cousin L, et al.: Molecular subgroups of atypical teratoid rhabdoid tumours in children: an integrated genomic and clinicopathological analysis. Lancet Oncol 16 (5): 569-82, 2015. [PUBMED Abstract]
  17. Johann PD, Erkek S, Zapatka M, et al.: Atypical Teratoid/Rhabdoid Tumors Are Comprised of Three Epigenetic Subgroups with Distinct Enhancer Landscapes. Cancer Cell 29 (3): 379-93, 2016. [PUBMED Abstract]
  18. Johann PD, Hovestadt V, Thomas C, et al.: Cribriform neuroepithelial tumor: molecular characterization of a SMARCB1-deficient non-rhabdoid tumor with favorable long-term outcome. Brain Pathol 27 (4): 411-418, 2017. [PUBMED Abstract]
  19. Frühwald MC, Hasselblatt M, Nemes K, et al.: Age and DNA methylation subgroup as potential independent risk factors for treatment stratification in children with atypical teratoid/rhabdoid tumors. Neuro Oncol 22 (7): 1006-1017, 2020. [PUBMED Abstract]
  20. Biegel JA, Fogelgren B, Wainwright LM, et al.: Germline INI1 mutation in a patient with a central nervous system atypical teratoid tumor and renal rhabdoid tumor. Genes Chromosomes Cancer 28 (1): 31-7, 2000. [PUBMED Abstract]
  21. Foulkes WD, Kamihara J, Evans DGR, et al.: Cancer Surveillance in Gorlin Syndrome and Rhabdoid Tumor Predisposition Syndrome. Clin Cancer Res 23 (12): e62-e67, 2017. [PUBMED Abstract]
  22. Wilson BG, Wang X, Shen X, et al.: Epigenetic antagonism between polycomb and SWI/SNF complexes during oncogenic transformation. Cancer Cell 18 (4): 316-28, 2010. [PUBMED Abstract]
  23. Knutson SK, Warholic NM, Wigle TJ, et al.: Durable tumor regression in genetically altered malignant rhabdoid tumors by inhibition of methyltransferase EZH2. Proc Natl Acad Sci U S A 110 (19): 7922-7, 2013. [PUBMED Abstract]
  24. Kurmasheva RT, Sammons M, Favours E, et al.: Initial testing (stage 1) of tazemetostat (EPZ-6438), a novel EZH2 inhibitor, by the Pediatric Preclinical Testing Program. Pediatr Blood Cancer 64 (3): , 2017. [PUBMED Abstract]
  25. Italiano A, Soria JC, Toulmonde M, et al.: Tazemetostat, an EZH2 inhibitor, in relapsed or refractory B-cell non-Hodgkin lymphoma and advanced solid tumours: a first-in-human, open-label, phase 1 study. Lancet Oncol 19 (5): 649-659, 2018. [PUBMED Abstract]

Treatment Treatment

There is limited information in the medical literature about the treatment of cramp-fasciculation syndrome (CFS). Much of what is available describes individual cases. Some people with CFS improve without treatment. Treatment with carbamazepine, gabapentin, lamotrigine, or pregabalin (medications that reduce the hyper-excitability of nerves) was described as helpful in improving symptoms in individual cases. Immunosuppressive therapy (e.g., prednisone ) has been used to treat cases of CFS that did not respond to other treatments. [3]

Decisions regarding treatment should be carefully considered and discussed with a knowledgeable healthcare provider.

  • mechanical injury during spinal surgery, or complications from spinal surgery (about 60% of cases)
  • trauma to the spinal cord
  • one or more spinal taps
  • steroid epidural injections or other injections
  • spinal and epidural anesthesia
  • bacterial or viral spinal infections

If you need medical advice, you can look for doctors or other healthcare professionals who have experience with this disease. You may find these specialists through advocacy organizations, clinical trials, or articles published in medical journals. You may also want to contact a university or tertiary medical center in your area, because these centers tend to see more complex cases and have the latest technology and treatments.

If you can’t find a specialist in your local area, try contacting national or international specialists. They may be able to refer you to someone they know through conferences or research efforts. Some specialists may be willing to consult with you or your local doctors over the phone or by email if you can't travel to them for care.

You can find more tips in our guide, How to Find a Disease Specialist. We also encourage you to explore the rest of this page to find resources that can help you find specialists.

Healthcare Resources

  • To find a medical professional who specializes in genetics, you can ask your doctor for a referral or you can search for one yourself. Online directories are provided by the American College of Medical Genetics and the National Society of Genetic Counselors. If you need additional help, contact a GARD Information Specialist. You can also learn more about genetic consultations from MedlinePlus Genetics.

Symptoms Symptoms

  • Eyes: Small eyes (microphthalmia), missing eyes (anophthalmia), absent or malformed lacrimal (tear) ducts, increased distance between the eyes (hypertelorism), vision loss
  • Face: Unusual hairline, missing eyebrows and/or eyelashes
  • Ears: Malformations of ear structure, hearing loss
  • Nose: Small, abnormally shaped nostrils, flattening of the top part of the nose (low nasal bridge)
  • Mouth: Cleft lip and palate, tooth crowding
  • Respiratory: Abnormal development of the voicebox (larynx) and trachea (windpipe), respiratory insufficiency
  • Chest and abdomen: Widely spaced nipples and umbilical abnormalities (umbilical hernia)
  • Genitourinary: Ambiguous genitalia, hypospadias (abnormal urethral opening in the penis), cryptorchidism (undescended testicle), absent or abnormal kidneys (renal agenesis or hypoplasia)
  • Skeletal: Separation of the pubic bones (diastasis of symphysis pubis), scoliosis , missing ribs
  • Neurologic: Small head size ( microcephaly ), spina bifida, intellectual disability

This table lists symptoms that people with this disease may have. For most diseases, symptoms will vary from person to person. People with the same disease may not have all the symptoms listed. This information comes from a database called the Human Phenotype Ontology (HPO) . The HPO collects information on symptoms that have been described in medical resources. The HPO is updated regularly. Use the HPO ID to access more in-depth information about a symptom.

Prevalence and Clinical Impact of Comorbid Anxiety and AUDs

Accuracy in prevalence estimates of comorbid anxiety and AUDs is essential for gauging the magnitude of the clinical and social impact of this comorbidity therefore, data should be carefully selected with attention to sampling methods. Information derived from clinical samples, although enlightening in its own right, produces inflated approximations of the prevalence of comorbidity (Kushner et al. 2008 Regier et al. 1990 Ross 1995). The most frequently offered explanation for the biased estimates from clinic-based samples suggests that individuals with multiple disorders are more likely to be referred for treatment than individuals with a single disorder (Galbaud Du Fort et al. 1993 Kushner et al. 2008). To avoid this bias, epidemiological data drawn from large-scale community samples can provide the most informative figures.

Over the past three decades, multiple population-based studies have surveyed the prevalence of addictive and mental disorders in the United States and abroad, including the following:

The Epidemiological Catchment Area (ECA) survey (Regier et al. 1990) was based on diagnostic information using the Diagnostic and Statistical Manual of Mental Disorders, Third Edition (DSM–III) (American Psychiatric Association [APA] 1980) it was conducted between 1980 and 1984 and collected information from nearly 20,000 respondents ages 18 and older in the United States.

The National Comorbidity Survey (NCS) (Kessler et al. 1994, 1997), also conducted in the United States, used the DSM–III–R criteria (APA 1987) while sampling 8,098 individuals ages 15 to 54 years.

Burns and Teesson (2002) published findings on the comorbidity between AUDs and anxiety, depression, and other drug use disorders from the Australian National Survey of Mental Health and Well-Being (NSMH&WB) project. This project was a cross-sectional analysis of 10,461 Australian adults ages 18 and older, with data collected in 1997 using diagnostic criteria from the DSM–IV (APA 1994).

The most recent epidemiological study to date, and the largest reviewed here, was the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) (Grant et al. 2004 Hasin et al. 2007). This survey, which was conducted by the National Institute on Alcohol Abuse and Alcoholism in 2001�, also applied DSM–IV diagnostic algorithms in a sample of 43,093 adults ages 18 and older.

The respective prevalences of comorbid anxiety disorders and AUDs from each of these epidemiological studies are summarized in table 1 . These data show that, across different large-scale studies, at different times, and both in the United States and abroad, anxiety and AUDs co-occur at rates greater than would be expected by chance alone. The odds ratios (ORs) characterizing the comorbidity between an AUD and any anxiety disorder in these studies ranged between 2.1 and 3.3—in other words, the two conditions co-occurred about two to three times as often as would be expected by chance alone.

Table 1

Adjusted Odds Ratios of the 12-Month Comorbidity Between Certain Anxiety Disorders and Alcohol Use Disorders Across Epidemiological Samples

Agoraphobia2. anxiety disorder—𠄼ompulsive disorder——2.7—Panic disorder4. phobia2.02.2—2.3Social phobia1.

NOTES: ECA = Epidemiologic Catchment Area Survey NCS = National Comorbidity Survey NSMH & WB = National Survey of Mental Health & Well-being NESARC = National Epidemiologic Survey on Alcohol and Related Conditions.

Three additional trends emerging from community-based samples are noteworthy. First, anxiety disorders are more strongly associated with alcohol dependence than with alcohol abuse (e.g., Hasin et al. 2007 Kessler et al. 1996 Kushner et al. 2008). Analysis of the NESARC data demonstrated that this finding generally was consistent across racial/ethnic groups (Smith et al. 2006). Alternative explanations for these results suggest that either people with anxiety disorders are more likely to become psychologically dependent on alcohol because they use it to self-medicate (e.g., Tran and Smith 2008) or anxiety disorders in these individuals largely are an artifact of alcohol withdrawal (e.g., Schuckit and Hesselbrock 1994).

Second, the magnitude of the relationship between specific anxiety disorders and AUDs varies across the specific combinations. For example, panic disorder typically has a relatively large association with AUDs (odds ratio [OR] = 1.7𠄴.1 in table 1 ), whereas obsessive-compulsive disorder has the least consistent and typically weakest relationship with alcohol problems (e.g., Gentil et al. 2009 Kessler et al. 1997 Schuckit et al. 1997 Torres et al. 2006). A classic review in this field (Kushner et al. 1990) indicated even more pronounced differences in the comorbidity rates of specific anxiety disorders among clinic-based samples of patients with alcohol problems. These ranged from rates near community-based rate estimates (e.g., for simple phobia) to rates nine times greater than community estimates (e.g., for social phobia). It is important to note, however, that the influence of treatment seeking and related variables confounds interpretation of these clinic-based estimates.

Third, different comorbidity patterns exist among patient subgroups with different demographic characteristics such as race/ethnicity and gender. For example, in the NESARC, Native Americans had elevated rates both of anxiety disorders and of AUDs over the past 12 months but lower rates of co-occurrence between these disorders compared with other ethnic groups (Smith et al. 2006). Gender differences in anxiety𠄺lcohol comorbidity have been reported across a variety of samples (e.g., Hesselbrock et al. 1985 Kessler et al. 1997 Mangrum et al. 2006 Merikangas et al. 1998), and research in this area also has identified notable clinical differences between men and women. These gender differences are discussed in more detail in the sidebar.

Gender Differences in Comorbid Anxiety and Alcohol Use Disorders

Numerous studies have attempted to evaluate possible gender differences in the frequency of comorbid anxiety disorders and alcohol use disorders (AUDs). Population surveys consistently show that anxiety disorders are more common among women, whereas AUDs are more common among men (e.g., Hasin et al. 2007 Kessler et al. 1997 Lewis et al. 1996). To account for these baserate differences when estimating gender-specific comorbidity rates for anxiety disorders and AUDs in the National Comorbidity Survey, Kessler and colleagues (1997) used adjusted odds ratios (ORs). These analyses found that among alcohol-dependent men in the sample, 35.8 percent (OR = 2.22) had a co-occurring anxiety disorder, compared with 60.7 percent (OR = 3.08) among alcohol-dependent women. Moreover, not only did women in the study have an increased likelihood of independent anxiety disorders compared with men, but prior anxiety disorders also were more strongly predictive of later alcohol dependence among the women. Furthermore, a multisite trial in Germany demonstrated that anxiety disorders had a substantial influence on the course and severity of alcoholism in women (Schneider et al. 2001). Thus, in this treatment-seeking sample women who had an anxiety disorder reported an accelerated temporal sequence of alcoholism, including earlier onset of first drink, regular drinking, and incidence of alcohol withdrawal than women with no anxiety disorder.

One potential explanation for these findings is that the reasons for using alcohol may differ by gender. For example, women may be more prone than men to self-medicate for mood problems with substances such as alcohol (Brady and Randall 1999). Furthermore, empirical inspection of gender differences in stress-related drinking has shown that women report higher levels of stress and have a stronger link between stress and drinking (Rice and Van Arsdale 2010 Timko et al. 2005). Together, these results suggest that women may be more likely to rely on alcohol to manage anxiety.

Anxiety disorders also may have a particularly detrimental impact on alcohol-focused treatment for women. This has been demonstrated in a series of studies evaluating the intersection of gender, social anxiety disorder, and treatment modality. Early work in this area from the Project MATCH sample revealed an intriguing interaction (Thevos et al. 2000). Specifically, whereas socially phobic men benefitted equally well from either cognitive�havioral therapy (CBT) or 12-step facilitation (TSF), women with social phobia fared less well if they were assigned to TSF. To shed light on the potential role of social anxiety in addiction treatment, Book and colleagues (2009) compared participants in an intensive outpatient program with high and low social anxiety on attitudes toward treatment activities. Members of the group with high social anxiety, who predominantly were female (71 percent), overall showed less treatment participation than did members of the comparison group. For example, they were less likely to speak up in group therapy, attend a 12-step meeting, or seek sponsorship within a 12-step group. A recent secondary analysis of alcoholics who were assigned to TSF in Project MATCH yielded findings consistent with and complementary to these observations, demonstrating that women with comorbid social phobia were 1.5 times more likely to relapse than noncomorbid women (Tonigan et al. 2010). In contrast, no differences in relapse rates were found among the men with or without social phobia in the study. Interestingly, socially phobic women were less likely than women without social phobia to obtain an Alcoholics Anonymous sponsor, which may help explain the poor outcomes for TSF among this subgroup.

Taken together, the findings reviewed here provide some instructive information on gender differences in the comorbidity of anxiety and AUDs. Thus, women are more likely than men to have both disorders, and the presence of anxiety disorders may exacerbate the course and severity of alcohol problems in women. Furthermore, treatment for women with this comorbidity may be especially complex, both because they are likely to use alcohol to self-medicate for stress and because women with social phobia may be reluctant to participate in treatment (e.g., Alcoholics Anonymous) that could otherwise be effective. These factors spotlight the importance of probing for anxiety disorders in women entering alcohol treatment and reinforce the need to remain sensitive to the different ways that gender can influence the process and outcomes of therapy.


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The importance of these prevalence data is underscored by the clinical impact of comorbid anxiety and AUDs. Both types of disorder are associated with substantial societal costs that have been estimated in monetary terms at $184.6 billion per year for AUDs (Harwood 2000) and between $42 and $47 billion for anxiety disorders (DuPont et al. 1996 Greenberg et al. 1999). Kessler and Greenberg (2002) suggested that the costs for anxiety disorders were grossly underestimated and actually exceeded $100 billion per year in the total U.S. population. Furthermore, clinical studies have shown that both anxiety and AUDs can negatively impact the course and treatment outcome for the other condition. For example, anxiety problems have been associated with increased severity and persistence of AUDs, increased risk for relapse following treatment, and increased lifetime service utilization in the context of substance use disorders more generally (Driessen et al. 2001 Falk et al. 2008 Kushner et al. 2005 Johnston et al. 1991 Perkonigg et al. 2006 Sannibale and Hall 2001). Conversely, concurrent AUDs have been associated with greater severity and chronicity of anxiety disorders, and substance use problems can decrease the likelihood of recovery from anxiety disorders (Bruce et al. 2005 Hornig and McNally 1995 Schade et al. 2004). Studies also have demonstrated that alcohol use can increase anxiety (see Kushner et al. 2000), which can result in a positive feedback loop leading to exacerbation of both disorders.

Taken together, the epidemiological and clinical literature describing the relationship between anxiety and AUDs shows that this comorbidity is both prevalent and clinically relevant. Therefore, it is important to enhance understanding of this comorbidity. The following sections will review fundamental concepts related to how these disorders co-occur and describe approaches to diagnosing and treating comorbid anxiety and AUDs.

According to research in the field of psychoneuroimmunology, upsetting thoughts and emotions may have a negative influence on health because of the link between the

Psychoneuroimmunology is the study of the effect of the mind on health and resistance to diseases. According to research in the field of psychoneuroimmunology, upsetting thoughts and emotions may have a negative influence on health because of the link between the brain and the immune system. Endocrine glands inside the body is responsible for many important functions and the hormones that this gland secretes have direct link with nervous system.

3.the immune system and the central nervous system are only remotely related to one another

Psychoneuroimmunology (PNI), also referred to as (PENI) or (PNEI), is the study of the interaction between psychological processes and the nervous and immune systems of the human body.[1] PNI takes an interdisciplinary approach, incorporating psychology, neuroscience, immunology, physiology, genetics, pharmacology, molecular biology, psychiatry, behavioral medicine, infectious diseases, endocrinology, and rheumatology.

The main interests of PNI are the interactions between the nervous and immune systems and the relationships between mental processes and health. PNI studies, among other things, the physiological functioning of the neuroimmune system in health and disease disorders of the neuroimmune system (autoimmune diseases hypersensitivities immune deficiency) and the physical, chemical and physiological characteristics of the components of the neuroimmune system in vitro, in situ, and in vivo.

The possible answers are :
1.lymphocytes themselves produce neurotransmitters and hormones.
2.the surfaces of lymphocytes contain receptor sites for neurotransmitters and hormones, including catecholamines and cortisol.
3.the immune system and the central nervous system are only remotely related to one another.
4.the central nervous system and the immune system are directly linked.

The answers 1 and 3 are not true.

The central nervous system and the immune system are directly linked and in constant communication. The central nervous system can trigger hormone and immune responses to various factors like stress, inflammation or neurological disease. The lymphocytes have receptors for neurotransmitters and hormones, but they can not produce them themselves.

35.2 Biogeography

In this section, you will explore the following questions:

  • What is biogeography?
  • What are examples of abiotic factors that affect the global distribution of plant and animal species?
  • What are examples of how abiotic factors can impact aquatic and terrestrial environments?
  • What are the effects of abiotic factors on net primary productivity?

Connection for AP ® Courses

Many forces influence the communities of living organisms present in different parts of the biosphere (all of the parts of Earth inhabited by life). The biosphere extends into the atmosphere (several kilometers above Earth) and into the depths of the oceans. Despite its apparent vastness to an individual human, the biosphere occupies only a minute space when compared to the known universe. Many abiotic forces influence where life can exist and the types of organisms found in different parts of the biosphere. The abiotic factors influence the distribution of biomes: large areas of land with similar climate, flora, and fauna.

Information presented and the examples highlighted in the section support concepts outlined in Big Idea 2 of the AP ® Biology Curriculum Framework. The AP ® Learning Objectives listed in the Curriculum Framework provide a transparent foundation for the AP ® Biology course, an inquiry-based laboratory experience, instructional activities, and AP ® exam questions. A learning objective merges required content with one or more of the seven science practices.

Big Idea 2 Biological systems utilize free energy and molecular building blocks to grow, to reproduce, and to maintain dynamic homeostasis.
Enduring Understanding 2.D Growth and dynamic homeostasis of a biological system are influenced by changes in the system’s environment.
Essential Knowledge 2.D.1 Populations, communities, and ecosystems are affected by interactions with abiotic factors in the environment.
Science Practice 1.3 The student can refine representations and models of natural or man-made phenomena and systems in the domain.
Science Practice 3.2 The student can refine scientific questions.
Learning Objective 2.22 The student is able to refine scientific models and questions about the effect of complex biotic and abiotic interactions on all biological systems, from cells and organisms to populations, communities, and ecosystems.
Essential Knowledge 2.D.1 Populations, communities, and ecosystems are affected by interactions with abiotic factors in the environment.
Science Practice 4.2 The student can design a plan for collecting data to answer a particular scientific question.
Science Practice 7.2 The student can connect concepts in and across domain(s) to generalize or extrapolate in and/or across enduring understandings and/or big ideas.
Learning Objective 2.23 The student is able to design a plan for collecting data to show that all biological systems are affected by complex biotic and abiotic interactions.
Essential Knowledge 2.D.1 Populations, communities, and ecosystems are affected by interactions with abiotic factors in the environment.
Science Practice 5.1 The student can analyze data to identify patterns or relationships.
Learning Objective 2.24 The student is able to analyze data to identify possible patterns and relationships between a biotic or abiotic factor and a biological system.


Biogeography is the study of the geographic distribution of living things and the abiotic factors that affect their distribution. Abiotic factors such as temperature and rainfall vary based mainly on latitude and elevation. As these abiotic factors change, the composition of plant and animal communities also changes. For example, if you were to begin a journey at the equator and walk north, you would notice gradual changes in plant communities. At the beginning of your journey, you would see tropical wet forests with broad-leaved evergreen trees, which are characteristic of plant communities found near the equator. As you continued to travel north, you would see these broad-leaved evergreen plants eventually give rise to seasonally dry forests with scattered trees. You would also begin to notice changes in temperature and moisture. At about 30 degrees north, these forests would give way to deserts, which are characterized by low precipitation.

Moving farther north, you would see that deserts are replaced by grasslands or prairies. Eventually, grasslands are replaced by deciduous temperate forests. These deciduous forests give way to the boreal forests found in the subarctic, the area south of the Arctic Circle. Finally, you would reach the Arctic tundra, which is found at the most northern latitudes. This trek north reveals gradual changes in both climate and the types of organisms that have adapted to environmental factors associated with ecosystems found at different latitudes. However, different ecosystems exist at the same latitude due in part to abiotic factors such as jet streams, the Gulf Stream, and ocean currents. If you were to hike up a mountain, the changes you would see in the vegetation would parallel those as you move to higher latitudes.

Ecologists who study biogeography examine patterns of species distribution. No species exists everywhere for example, the Venus flytrap is endemic to a small area in North and South Carolina. An endemic species is one which is naturally found only in a specific geographic area that is usually restricted in size. Other species are generalists: species which live in a wide variety of geographic areas the raccoon, for example, is native to most of North and Central America.

Species distribution patterns are based on biotic and abiotic factors and their influences during the very long periods of time required for species evolution therefore, early studies of biogeography were closely linked to the emergence of evolutionary thinking in the eighteenth century. Some of the most distinctive assemblages of plants and animals occur in regions that have been physically separated for millions of years by geographic barriers. Biologists estimate that Australia, for example, has between 600,000 and 700,000 species of plants and animals. Approximately 3/4 of living plant and mammal species are endemic species found solely in Australia (Figure 35.6ab).

Sometimes ecologists discover unique patterns of species distribution by determining where species are not found. Hawaii, for example, has no native land species of reptiles or amphibians, and has only one native terrestrial mammal, the hoary bat. Most of New Guinea, as another example, lacks placental mammals.

Link to Learning

Check out this video to observe a platypus swimming in its natural habitat in New South Wales, Australia.

Plants can be endemic or generalists: endemic plants are found only on specific regions of the Earth, while generalists are found on many regions. Isolated land masses—such as Australia, Hawaii, and Madagascar—often have large numbers of endemic plant species. Some of these plants are endangered due to human activity. The forest gardenia (Gardenia brighamii), for instance, is endemic to Hawaii only an estimated 15–20 trees are thought to exist (Figure 35.7).

Science Practice Connection for AP® Courses

Think About It

Many endemic species are found in areas that are geographically isolated. What is a possible scientific explanation for this observation? Justify your answer.

Use The College Board Advanced Placement Program: Measuring Primary Productivity—Grass Plants: Student Lab Template, found here to explore the concept of primary productivity versus gross productivity. You will calculate primary productivity, be introduced to the benefits of measuring dry mass versus wet mass, and make predictions about the changes in net primary productivity based on the variables you decide to focus on.

To learn more about calculating net primary productivity, watch this video.

Teacher Support

  • The Think About It question is an application of AP ® Learning Objective 2.24 and Science Practice 5.1 because students are asked to draw conclusions (explanations) from observable data.
  • Sample Answer for Think About It question: Isolated species experience genetic drift, a random change in allele frequency in a population. In a small enough population that does not interbreed other populations of the same species, the differences add up over a long period of time and can create a new species. Geographical isolation ensures there will be no influx of genetic information from the original species to inhibit the evolution of a new species uniquely suited to its location.
  • The lab investigation is an application of AP ® Learning Objective 2.24 and Science Practices 1.3, 3.2, 5.1, and 7.2 because students will make predictions about natural phenomena, design experiments to test the effects of different variables, evaluate evidence provided by the data, use data to perform calculations, and use that information to support a conclusion. Teacher resources for this lab are in The College Board Advanced Placement Program: Measuring Primary Productivity—Teacher Lab Template, found here.

Energy Sources

Energy from the sun is captured by green plants, algae, cyanobacteria, and photosynthetic protists. These organisms convert solar energy into the chemical energy needed by all living things. Light availability can be an important force directly affecting the evolution of adaptations in photosynthesizers. For instance, plants in the understory of a temperate forest are shaded when the trees above them in the canopy completely leaf out in the late spring. Not surprisingly, understory plants have adaptations to successfully capture available light. One such adaptation is the rapid growth of spring ephemeral plants such as the spring beauty (Figure 35.8). These spring flowers achieve much of their growth and finish their life cycle (reproduce) early in the season before the trees in the canopy develop leaves.

In aquatic ecosystems, the availability of light may be limited because sunlight is absorbed by water, plants, suspended particles, and resident microorganisms. Toward the bottom of a lake, pond, or ocean, there is a zone that light cannot reach. Photosynthesis cannot take place there and, as a result, a number of adaptations have evolved that enable living things to survive without light. For instance, aquatic plants have photosynthetic tissue near the surface of the water for example, think of the broad, floating leaves of a water lily—water lilies cannot survive without light. In environments such as hydrothermal vents, some bacteria extract energy from inorganic chemicals because there is no light for photosynthesis.

The availability of nutrients in aquatic systems is also an important aspect of energy or photosynthesis. Many organisms sink to the bottom of the ocean when they die in the open water when this occurs, the energy found in that living organism is sequestered for some time unless ocean upwelling occurs. Ocean upwelling is the rising of deep ocean waters that occurs when prevailing winds blow along surface waters near a coastline (Figure 35.9). As the wind pushes ocean waters offshore, water from the bottom of the ocean moves up to replace this water. As a result, the nutrients once contained in dead organisms become available for reuse by other living organisms.

In freshwater systems, the recycling of nutrients occurs in response to air temperature changes. The nutrients at the bottom of lakes are recycled twice each year: in the spring and fall turnover. The spring and fall turnover is a seasonal process that recycles nutrients and oxygen from the bottom of a freshwater ecosystem to the top of a body of water (Figure 35.10). These turnovers are caused by the formation of a thermocline: a layer of water with a temperature that is significantly different from that of the surrounding layers. In wintertime, the surface of lakes found in many northern regions is frozen. However, the water under the ice is slightly warmer, and the water at the bottom of the lake is warmer yet at 4 °C to 5 °C (39.2 °F to 41 °F). Water is densest at 4 °C therefore, the deepest water is also the densest. The deepest water is oxygen poor because the decomposition of organic material at the bottom of the lake uses up available oxygen that cannot be replaced by means of oxygen diffusion into the water due to the surface ice layer.

Visual Connection

  1. Spring turnover occurs in tropical lakes, but not in temperate lakes. Stratification occurs in temperate lakes.
  2. Temperate lakes do not freeze so they do not undergo spring turnover or stratification.
  3. Stratification and spring turnover occur in tropical lakes. Temperate lakes do not freeze so they do not undergo spring turnover.
  4. Stratification and spring turnover occur in temperate lakes. Tropical lakes do not freeze so they do not undergo spring turnover.

In springtime, air temperatures increase and surface ice melts. When the temperature of the surface water begins to reach 4 °C, the water becomes heavier and sinks to the bottom. The water at the bottom of the lake is then displaced by the heavier surface water and, thus, rises to the top. As that water rises to the top, the sediments and nutrients from the lake bottom are brought along with it. During the summer months, the lake water stratifies, or forms layers, with the warmest water at the lake surface.

As air temperatures drop in the fall, the temperature of the lake water cools to 4 °C therefore, this causes fall turnover as the heavy cold water sinks and displaces the water at the bottom. The oxygen-rich water at the surface of the lake then moves to the bottom of the lake, while the nutrients at the bottom of the lake rise to the surface (Figure 35.10). During the winter, the oxygen at the bottom of the lake is used by decomposers and other organisms requiring oxygen, such as fish.


Temperature affects the physiology of living things as well as the density and state of water. Temperature exerts an important influence on living things because few living things can survive at temperatures below 0 °C (32 °F) due to metabolic constraints. It is also rare for living things to survive at temperatures exceeding 45 °C (113 °F) this is a reflection of evolutionary response to typical temperatures. Enzymes are most efficient within a narrow and specific range of temperatures enzyme degradation can occur at higher temperatures. Therefore, organisms either must maintain an internal temperature or they must inhabit an environment that will keep the body within a temperature range that supports metabolism. Some animals have adapted to enable their bodies to survive significant temperature fluctuations, such as seen in hibernation or reptilian torpor. Similarly, some bacteria are adapted to surviving in extremely hot temperatures such as geysers. Such bacteria are examples of extremophiles: organisms that thrive in extreme environments.

Temperature can limit the distribution of living things. Animals faced with temperature fluctuations may respond with adaptations, such as migration, in order to survive. Migration, the movement from one place to another, is an adaptation found in many animals, including many that inhabit seasonally cold climates. Migration solves problems related to temperature, locating food, and finding a mate. In migration, for instance, the Arctic Tern (Sterna paradisaea) makes a 40,000 km (24,000 mi) round trip flight each year between its feeding grounds in the southern hemisphere and its breeding grounds in the Arctic Ocean. Monarch butterflies (Danaus plexippus) live in the eastern United States in the warmer months and migrate to Mexico and the southern United States in the wintertime. Some species of mammals also make migratory forays. Reindeer (Rangifer tarandus) travel about 5,000 km (3,100 mi) each year to find food. Amphibians and reptiles are more limited in their distribution because they lack migratory ability. Not all animals that can migrate do so: migration carries risk and comes at a high energy cost.

Some animals hibernate or estivate to survive hostile temperatures. Hibernation enables animals to survive cold conditions, and estivation allows animals to survive the hostile conditions of a hot, dry climate. Animals that hibernate or estivate enter a state known as torpor: a condition in which their metabolic rate is significantly lowered. This enables the animal to wait until its environment better supports its survival. Some amphibians, such as the wood frog (Rana sylvatica), have an antifreeze-like chemical in their cells, which retains the cells’ integrity and prevents them from bursting.


Water is required by all living things because it is critical for cellular processes. Since terrestrial organisms lose water to the environment by simple diffusion, they have evolved many adaptations to retain water.

  • Plants have a number of interesting features on their leaves, such as leaf hairs and a waxy cuticle, that serve to decrease the rate of water loss via transpiration.
  • Freshwater organisms are surrounded by water and are constantly in danger of having water rush into their cells because of osmosis. Many adaptations of organisms living in freshwater environments have evolved to ensure that solute concentrations in their bodies remain within appropriate levels. One such adaptation is the excretion of dilute urine.
  • Marine organisms are surrounded by water with a higher solute concentration than the organism and, thus, are in danger of losing water to the environment because of osmosis. These organisms have morphological and physiological adaptations to retain water and release solutes into the environment. For example, Marine iguanas (Amblyrhynchus cristatus), sneeze out water vapor that is high in salt in order to maintain solute concentrations within an acceptable range while swimming in the ocean and eating marine plants.

Inorganic Nutrients and Soil

Inorganic nutrients, such as nitrogen and phosphorus, are important in the distribution and the abundance of living things. Plants obtain these inorganic nutrients from the soil when water moves into the plant through the roots. Therefore, soil structure (particle size of soil components), soil pH, and soil nutrient content play an important role in the distribution of plants. Animals obtain inorganic nutrients from the food they consume. Therefore, animal distributions are related to the distribution of what they eat. In some cases, animals will follow their food resource as it moves through the environment.

Other Aquatic Factors

Some abiotic factors, such as oxygen, are important in aquatic ecosystems as well as terrestrial environments. Terrestrial animals obtain oxygen from the air they breathe. Oxygen availability can be an issue for organisms living at very high elevations, however, where there are fewer molecules of oxygen in the air. In aquatic systems, the concentration of dissolved oxygen is related to water temperature and the speed at which the water moves. Cold water has more dissolved oxygen than warmer water. In addition, salinity, current, and tide can be important abiotic factors in aquatic ecosystems.

Other Terrestrial Factors

Wind can be an important abiotic factor because it influences the rate of evaporation and transpiration. The physical force of wind is also important because it can move soil, water, or other abiotic factors, as well as an ecosystem’s organisms.

Fire is another terrestrial factor that can be an important agent of disturbance in terrestrial ecosystems. Some organisms are adapted to fire and, thus, require the high heat associated with fire to complete a part of their life cycle. For example, the jack pine—a coniferous tree—requires heat from fire for its seed cones to open (Figure 35.11). Through the burning of pine needles, fire adds nitrogen to the soil and limits competition by destroying undergrowth.

Abiotic Factors Influencing Plant Growth

Temperature and moisture are important influences on plant production (primary productivity) and the amount of organic matter available as food (net primary productivity). Net primary productivity is an estimation of all of the organic matter available as food it is calculated as the total amount of carbon fixed per year minus the amount that is oxidized during cellular respiration. In terrestrial environments, net primary productivity is estimated by measuring the aboveground biomass per unit area, which is the total mass of living plants, excluding roots. This means that a large percentage of plant biomass which exists underground is not included in this measurement. Net primary productivity is an important variable when considering differences in biomes. Very productive biomes have a high level of aboveground biomass.

Annual biomass production is directly related to the abiotic components of the environment. Environments with the greatest amount of biomass have conditions in which photosynthesis, plant growth, and the resulting net primary productivity are optimized. The climate of these areas is warm and wet. Photosynthesis can proceed at a high rate, enzymes can work most efficiently, and stomata can remain open without the risk of excessive transpiration together, these factors lead to the maximal amount of carbon dioxide (CO2) moving into the plant, resulting in high biomass production. The aboveground biomass produces several important resources for other living things, including habitat and food. Conversely, dry and cold environments have lower photosynthetic rates and therefore less biomass. The animal communities living there will also be affected by the decrease in available food.

Understory plants in a temperate forest have adaptations to capture limited ________.

An ecologist hiking up a mountain may notice different biomes along the way due to changes in all of the following except:

Compare and contrast ocean upwelling and spring and fall turnovers.

Ocean upwelling is a continual process that occurs year-round. Spring and fall turnover in freshwater lakes and ponds, however, is a seasonal process that occurs due to temperature changes in the water that take place during springtime warming and autumn cooling. Both ocean upwelling and spring and fall turnover enable nutrients in the organic materials at the bottom of the body of water to be recycled and reused by living things.

Many endemic species are found in areas that are geographically isolated. Suggest a plausible scientific explanation for why this is so.

Areas that have been geographically isolated for very long periods of time allow unique species to evolve these species are distinctly different from those of surrounding areas and remain so, since geographic isolation keeps them separated from other species.

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