Dementia pathophysiology: Difference between revisions
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*Deteriorating course over up to 8-10 years. | *Deteriorating course over up to 8-10 years. | ||
*Brain lesions are marked by neurofibrillary tangles, senile plaques, neuronal loss, and brain atrophy, with defects in acetylcholine synthesis at the cellular level. | *Brain lesions are marked by neurofibrillary tangles, senile plaques, neuronal loss, and brain atrophy, with defects in acetylcholine synthesis at the cellular level. | ||
*The ultimate neurotoxin in dementia is debated, but experimental evidence highlights small aggregates of amyloid beta peptides called oligomers, as opposed to larger aggregates called fibril | *The ultimate neurotoxin in dementia is debated, but experimental evidence highlights small aggregates of amyloid beta peptides called oligomers, as opposed to larger aggregates called fibril<ref name="pmid28882996">{{cite journal |vauthors=Gremer L, Schölzel D, Schenk C, Reinartz E, Labahn J, Ravelli RBG, Tusche M, Lopez-Iglesias C, Hoyer W, Heise H, Willbold D, Schröder GF |title=Fibril structure of amyloid-β(1-42) by cryo-electron microscopy |journal=Science |volume=358 |issue=6359 |pages=116–119 |date=October 2017 |pmid=28882996 |doi=10.1126/science.aao2825 |url=}}</ref> | ||
Revision as of 16:35, 8 October 2020
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Dementia Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: ,Sabeeh Islam, MBBS[2]
Overview
- Chronic, progressive neurodegenerative disorder characterized by a global, nonreversible impairment in cerebral functioning.
- Deteriorating course over up to 8-10 years.
- Brain lesions are marked by neurofibrillary tangles, senile plaques, neuronal loss, and brain atrophy, with defects in acetylcholine synthesis at the cellular level.
- The ultimate neurotoxin in dementia is debated, but experimental evidence highlights small aggregates of amyloid beta peptides called oligomers, as opposed to larger aggregates called fibril[1]
Pathophysiology
While the pathogenesis of AD remains unclear, It is thought that dementia is the result of
- Overproduction and/or decreased clearance of amyloid beta peptides
- Accumulation of tau proteins
- Accumulation of neurofibrillary tangles
- Production of oxygen radicals and nitric oxide, and inflammatory processes
- Decreased levels of cholinergic neurotransmission.
- Over-excitation of the glutamate neurotransmitter system via N-methyl-D-aspartate receptors
These changes are usually present in the hippocampus, amygdala, cortex, and nucleus basalis
Genes
Genes involved in the pathogenesis of dementia include
- Amyloid precursor protein (APP)
- Presenilin 1 (PSEN1)[2]
- Presenilin 2 (PSEN2)
- Apolipoprotein E (APOE)
- C9ORF72
- MAPT
- GRN[3]
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Dementia Microchapters |
References
- ↑ Gremer L, Schölzel D, Schenk C, Reinartz E, Labahn J, Ravelli R, Tusche M, Lopez-Iglesias C, Hoyer W, Heise H, Willbold D, Schröder GF (October 2017). "Fibril structure of amyloid-β(1-42) by cryo-electron microscopy". Science. 358 (6359): 116–119. doi:10.1126/science.aao2825. PMID 28882996. Vancouver style error: initials (help)
- ↑ Whooley MA, Avins AL, Miranda J, Browner WS (July 1997). "Case-finding instruments for depression. Two questions are as good as many". J Gen Intern Med. 12 (7): 439–45. doi:10.1046/j.1525-1497.1997.00076.x. PMC 1497134. PMID 9229283.
- ↑ Arroll B, Khin N, Kerse N (November 2003). "Screening for depression in primary care with two verbally asked questions: cross sectional study". BMJ. 327 (7424): 1144–6. doi:10.1136/bmj.327.7424.1144. PMC 261815. PMID 14615341.