Alzheimer's disease Flashcards
What are the symptoms of AD
memory loss, impaired ability to learn, imparied ability to carry out daily activites, anxiety, suspicion, hallucinations, motor dysfunction
What are environmental and genetic factors associated with elevated AD risk
age
low education
reduced mental activity in late life
reduced physical activity in late life
risk for vascular disease
head injury
How is the amyloid-beta peptide generated
Abeta is a smaller peptibe that is cleaved from a larger prtoein known as APP gene which leads to plaques
- clevage in the mutated in APP causes greater production of more Abeta42 vs Abeta40
Understand how ApoE genetic status modulates AD risk.
ApoE is responsible for transporting cholesterol into the brain and an altered ApoE function can affect Abeta aggregation or clearence
Describe the role of cholinesterase inhibitors agents in AD therapy.
These drugs work by blocking acetylcholine esterase and compensate for the loss of acetylcholine that results from the degeneration of cholinergic nerve terminals in AD
Drugs in this class include
Donepezil
Rivastigmine
Glantamine
Describe pathogenic mechanisms being targeted in the development of new AD therapies.
AB generation
AB aggregation
AB clearance
Tau kinase inhibitors
Glutamate-mediated excitotoxicity
Inflammation or oxidative stress
Understand how Florbetapir (18F) and other imaging agents can be used to monitor amyloid formation in living individuals.
Florbetapir is a radiolabeled agent that binds to B-amilyoid and can be visualized on a PET scan.
Know similarities and differences between AD and other dementias (DLB, FTDP).
Vascular dementia - impaired judgment or executive function, brain injury associated with vascular disease or stroke
Dementia with lewy bodies - combination of cognitive decline and parkinsonian symptoms, visual hallucinations
Frontotemporal dementia - disinhibited behavior, tau accumulation
Amyloid plaques vs neueofibrillary tangles
Amyloid plaques are extracellullar and consist of amyloid beta peptide
neurofibrils are intracellular and consist of hyper-phosphrylated tau
Describe the role of anti- glutamatergic agents in AD therapy.
these drugs work to reduce excitotoxicity by blocking glutamatergic neurotransmission via a noncompetitive mechanism