Alzheimer's disease causes: Difference between revisions

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{{CMG}}
__NOTOC__
{{Alzheimer's disease}}
{{Alzheimer's disease}}


{{CMG}}; {{AE}} {{HK}}
==Overview==
==Overview==
The cause of Alzheimer's disease is poorly understood. Research indicates that the disease is associated with [[Senile plaques|plaques]] and [[neurofibrillary tangles|tangles]] in the [[brain]].<ref name="pmid15184601">{{cite journal |author=Tiraboschi P, Hansen LA, Thal LJ, Corey-Bloom J |title=The importance of neuritic plaques and tangles to the development and evolution of AD |journal=[[Neurology]] |volume=62 |issue=11 |pages=1984–9 |year=2004 |month=June |pmid=15184601 |doi= |url=http://www.neurology.org/cgi/pmidlookup?view=long&pmid=15184601 |accessdate=2012-08-16}}</ref>
Alzheimer's disease may be caused by [[Trisomy 21|trisomy of chromosome 21]], [[familial]] [[inheritance]] of [[mutations]] in either [[Presenilin 1|presenilin 1 gene]], [[Presenilin|presenilin 2 gene]] or [[APOE|APOE4]] [[gene]]. [[Presenilin]] [[mutations]] are associated with early onset Alzheimer's disease, whereas [[APOE]] [[mutations]] are associated with late onset disease. Environmental factors, such as [[aging]], low level of education and head [[trauma]] may also contribute to the development of Alzheimer's disease.
 
==Causes==
 
The following are the causes of Alzheimer's dementia (AD):<ref name="urlAlzheimer Disease Overview - GeneReviews® - NCBI Bookshelf">{{cite web |url=https://www.ncbi.nlm.nih.gov/books/NBK1161/ |title=Alzheimer Disease Overview - GeneReviews® - NCBI Bookshelf |format= |work= |accessdate=}}</ref><ref name="pmid16966510">{{cite journal |vauthors=Brickell KL, Steinbart EJ, Rumbaugh M, Payami H, Schellenberg GD, Van Deerlin V, Yuan W, Bird TD |title=Early-onset Alzheimer disease in families with late-onset Alzheimer disease: a potential important subtype of familial Alzheimer disease |journal=Arch. Neurol. |volume=63 |issue=9 |pages=1307–11 |year=2006 |pmid=16966510 |doi=10.1001/archneur.63.9.1307 |url=}}</ref><ref name="pmid10441572">{{cite journal |vauthors=Campion D, Dumanchin C, Hannequin D, Dubois B, Belliard S, Puel M, Thomas-Anterion C, Michon A, Martin C, Charbonnier F, Raux G, Camuzat A, Penet C, Mesnage V, Martinez M, Clerget-Darpoux F, Brice A, Frebourg T |title=Early-onset autosomal dominant Alzheimer disease: prevalence, genetic heterogeneity, and mutation spectrum |journal=Am. J. Hum. Genet. |volume=65 |issue=3 |pages=664–70 |year=1999 |pmid=10441572 |pmc=1377972 |doi=10.1086/302553 |url=}}</ref><ref name="pmid11216203">{{cite journal |vauthors=Munoz DG, Feldman H |title=Causes of Alzheimer's disease |journal=CMAJ |volume=162 |issue=1 |pages=65–72 |year=2000 |pmid=11216203 |pmc=1232234 |doi= |url=}}</ref><ref name="pmid9848086">{{cite journal |vauthors=Hölscher C |title=Possible causes of Alzheimer's disease: amyloid fragments, free radicals, and calcium homeostasis |journal=Neurobiol. Dis. |volume=5 |issue=3 |pages=129–41 |year=1998 |pmid=9848086 |doi=10.1006/nbdi.1998.0193 |url=}}</ref>
{| class="wikitable"
! align="center" style="background:#4479BA; color: #FFFFFF;" + |'''Cause'''
! align="center" style="background:#4479BA; color: #FFFFFF;" + |'''Specific characteristics'''
! align="center" style="background:#4479BA; color: #FFFFFF;" + |'''Percentage of cases'''
|-
| colspan="1" rowspan="1" |'''[[Chromosomal]] ([[Down syndrome]])'''
|
* [[Trisomy 21]]
* Over expression of [[amyloid precursor protein]] ([[Amyloid precursor protein|APP]]) on [[Chromosome 21 (human)|chromosome 21]] 
* Develop the neuropathologic hallmarks of AD after age 40 years
| colspan="1" rowspan="1" |<1%
|-
| colspan="1" rowspan="1" |'''All familial'''
|
| colspan="1" rowspan="1" |~25%
|-
| colspan="1" rowspan="1" |
* Late-onset familial (AD2)
|
* [[APOE]] [[gene]]:
** [[Locus]]: AD2
** [[Protein]]: [[Apolipoprotein E]]
* TREM2 [[gene]]:
** Variant: p.Arg47His [[Allele|allelic]] variant
* PLD3 [[gene]]
* UNC5C [[gene]]
* [[AKAP9]] [[gene]]:
** In African-Americans only
| colspan="1" rowspan="1" |15%-25% of [[familial]] cases
|-
| colspan="1" rowspan="1" |
* Early-onset familial AD (AD1, AD3, AD4)
|
* [[PSEN1]] [[gene]]:
** [[Locus]]: AD3
** Proportion: 20-70 % of early onset AD cases
** [[Protein]]: [[Presenilin 1|Presenilin-1]]
* [[PSEN2]] [[gene]]:
** [[Locus]]: AD4
** Proportion: Rare
** [[Protein]]: [[Presenilin|Presenilin-2]]
* [[Amyloid precursor protein|APP]] [[gene]]:
** [[Locus]]: AD1
** Proportion: 10-15 % of early onset AD cases
** [[Protein]]: [[Amyloid precursor protein]] ([[Amyloid precursor protein|APP]])
| colspan="1" rowspan="1" |<2% of [[familial]] cases
|-
| colspan="1" rowspan="1" |'''Unknown (includes genetic/environment interactions)'''
|
* Multifactorial: (combination of)
** [[Aging]]
** [[Genetic predisposition]]
** Exposure to one or more environmental agents including head [[trauma]], low education level, [[viruses]], and/or [[toxins]]
| colspan="1" rowspan="1" |~75%
|}


==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
{{WS}}
{{WH}}
[[Category:Psychiatry]]
[[Category:Neurology]]

Latest revision as of 15:54, 21 September 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Overview

Alzheimer's disease may be caused by trisomy of chromosome 21, familial inheritance of mutations in either presenilin 1 gene, presenilin 2 gene or APOE4 gene. Presenilin mutations are associated with early onset Alzheimer's disease, whereas APOE mutations are associated with late onset disease. Environmental factors, such as aging, low level of education and head trauma may also contribute to the development of Alzheimer's disease.

Causes

The following are the causes of Alzheimer's dementia (AD):[1][2][3][4][5]

Cause Specific characteristics Percentage of cases
Chromosomal (Down syndrome) <1%
All familial ~25%
  • Late-onset familial (AD2)
 15%-25% of familial cases
  • Early-onset familial AD (AD1, AD3, AD4)
 <2% of familial cases
Unknown (includes genetic/environment interactions) ~75%

References

  1. ↑ "Alzheimer Disease Overview - GeneReviews® - NCBI Bookshelf".
  2. ↑ Brickell KL, Steinbart EJ, Rumbaugh M, Payami H, Schellenberg GD, Van Deerlin V, Yuan W, Bird TD (2006). "Early-onset Alzheimer disease in families with late-onset Alzheimer disease: a potential important subtype of familial Alzheimer disease". Arch. Neurol. 63 (9): 1307–11. doi:10.1001/archneur.63.9.1307. PMID 16966510.
  3. ↑ Campion D, Dumanchin C, Hannequin D, Dubois B, Belliard S, Puel M, Thomas-Anterion C, Michon A, Martin C, Charbonnier F, Raux G, Camuzat A, Penet C, Mesnage V, Martinez M, Clerget-Darpoux F, Brice A, Frebourg T (1999). "Early-onset autosomal dominant Alzheimer disease: prevalence, genetic heterogeneity, and mutation spectrum". Am. J. Hum. Genet. 65 (3): 664–70. doi:10.1086/302553. PMC 1377972. PMID 10441572.
  4. ↑ Munoz DG, Feldman H (2000). "Causes of Alzheimer's disease". CMAJ. 162 (1): 65–72. PMC 1232234. PMID 11216203.
  5. ↑ Hölscher C (1998). "Possible causes of Alzheimer's disease: amyloid fragments, free radicals, and calcium homeostasis". Neurobiol. Dis. 5 (3): 129–41. doi:10.1006/nbdi.1998.0193. PMID 9848086.

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