Dementia pathophysiology: Difference between revisions
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{{CMG}};{{AE}},{{SAI}} | {{CMG}};{{AE}},{{SAI}} | ||
== Overview == | ==Overview== | ||
== Pathophysiology == | ==Pathophysiology== | ||
<br />__NOTOC__ | 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 | |||
<br /> | |||
__NOTOC__ | |||
{{Template:Dementia}} | {{Template:Dementia}} | ||
== References == | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
{{WH}} | {{WH}} |
Revision as of 23:15, 28 September 2020
Dementia Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: ,Sabeeh Islam, MBBS[2]
Overview
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
Dementia Microchapters |