Alzheimer's Disease Flashcards
(16 cards)
1
Q
cause -familial AD
A
- rare but common in early onset
- changes happen more rapidly
- clear genetic basis
- Mutations to 3 different genes - all show autosomal dominance
- children of indius with familial AD have 50% of dev AD
2
Q
Familial AD gene
A
- found on chromosomes : 1, 14 +21
- presenilin 1,2 + Amyloid beta precursor protein
each mutation causes build of amyloid plaques - genetic testing can identify whether indiv carries the mutant form
3
Q
causes- Late onset AD
A
- 99% of people with AD have late onset
- 1 gene implicated - apolipoproteing
-1 copy of the gene increases AD risk by 4 2 copies = 10-20
4
Q
Environmental factors /Lifestyle
A
- Diets with high fat conc increase risk
- Diets with lots of fruit, veg. fish decrease risk of AD
- Interaction between diet genetics - larger effect of diet at higher genetic risk
- smoking increases risk of apolipoproteing gene associated with late onset
- Neuroinflammation
5
Q
modifiable Risk factors
A
- 45% of cases of dementia potentially preventable by modifying risk factors :
- lower levels of ed, hearing impairment, high cholesterol, TB I , physical inactivity, diabetes, Smoking,obesity
6
Q
Diagnosis - How early can we detect AD
A
- Has insidious onset (hard to notice at first, increases with age)
- symptoms of mild cog impairment (MCI) : losing train of thought, difficulty remembering appointments, misplacing everyday items
7
Q
Difference between MCI +AD
A
- AD Must : increasing deficits in 2 + areas of cog , severe problems interfering with everyday activities
- MCI for milder deficit - may reflect early stage of AD
- 12 % of people with MCI dev dementia that year
- 50%. of those with der dementia after 5 years
- Defrancesco et al
8
Q
MCI + brain structures
A
- Brain imaging shows degeneration of hippocampus + other memory structures in MCl patients 3 years before AD diagnosis
9
Q
cog Reserve - intelligence
A
- High levels of intelligence + education may allow an indie to function relatively normally through early stages of AD
- Neural functioning does gradually decline
10
Q
Evidence that education effects AD onset
A
- The Nun study- > Kemper et al
- Nuns who developed dementia showed lower scores of density of ideas + grammatical complexity
- Eclipse study -> Brain
- Those who had higher levels of ed where less likely to be diagnosed with AD even though had same level of plaques + tangles as those with AD
- shows higher ed enabled them to still function adequately
11
Q
can AD be treated
A
- cog stimulations, exercise + improved nutrition can boost performance + mood for people with AD
- Reminiscence therapy allows patients to make best use of early memories + knowledge
- showing cues that may link to past memories
- earliest memories are most resilient against pathology
12
Q
power of music in treating AD
A
- Before music lady with AD was sat in the chair unresponsive
- professional balIerine + when music played she remembered the routine + provoked a convo about point shoes
13
Q
Mild to moderate stages treatment
A
- cholinesterase inhibitors
- drugs boost acetescholine levels
- Half show benefits in cog after taking them
14
Q
moderate to severe stages treatment
A
- NMDA inhibitors
- Drugs block glutamate which is released in large quantities by damaged cells + is toxic
- Anti-AD drugs don’t stop progression + only work on some patients, are expensive + have sig side effects
15
Q
Immunotherapy treatment
A
-Harnessing immune system to reduce amyloid plaques
- New drugs involve monoclonal antibodies that target + remove beta amyloid
- Antibodies stick proteins in AD brain
- Antibodies attract immune cells ten break down protein
16
Q
Lecanemab trial
A
- 2022 trial of anti-amyloid antibodies
- Infusion 2 a week over 18 months VS placebo
- worked to reduce amyloid antibodies
- very serious side effects in 3% - brain swelling + bleeds
