Alzheimer's disease Flashcards

1
Q

What is AD?

A

Serious loss of cognitive ability due to amyloid beta plaque formation

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2
Q

What are the symptoms

A

Loss of memory, attention, language, problem solving and cognitive abilities

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3
Q

What are the details about the APOE genes

A

3 is normal risk
2 is reduced risk
4 is increased risk

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4
Q

What are the cellular halmarks?

A

Amyloid beta plaque formation and hyperphosphorilation of tau

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5
Q

How are amyloid beta plaques formed?

A

Normally, alpha and beta secretase cut amyloid fragments. If instead beta and gamma do this, a toxic form is created that accumulates in the brain, causing neural degradation

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6
Q

Explain how tau causes AD

A

Tau regulates the stability of microtubules in the brain. If it gets hyperphosphorilated, Microtubules get destabilized, become fragmented and form tangles

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7
Q

What are other AD pathologies?

A

Cholinergic dysfunction - Cholinergic deficit may lead to AD
Inflammation
Clearance problems (RAGE-LRP) LRP clears abeta from the brain, RAGE imports it. So LRP is dysfunctional
Cholesterol metabolism - High cholesterol increases the chance of abeta deposition
Insulin dysfunction - Insulin dysfunction triggers amyloid beta formation (diabetis T3)
Direct infection

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8
Q

How do we treat plaque formation?

A

With beta secretase inhibitors such as rosiglitazone

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9
Q

How do we treat the cholinergic defecit

A

With AchE-i such as donepezil, rivastigmin and galantamin.

Also with NMDAi memantine

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10
Q

How do we treat Tau?

A

With methylene blue

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