Dementia pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
* Chronic, progressive neurodegenerative disorder characterized by a global, nonreversible impairment in cerebral functioning. | *Chronic, progressive neurodegenerative disorder characterized by a global, nonreversible impairment in cerebral functioning. | ||
* 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 | |||
Revision as of 16:34, 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
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)[1]
- Presenilin 2 (PSEN2)
- Apolipoprotein E (APOE)
- C9ORF72
- MAPT
- GRN[2]
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Dementia Microchapters |
References
- ↑ 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.