Biopsychology: Alzhiemer Disease Flashcards

1
Q

Statement on ad and how it is increasing

A

Ad is growing in the population due to increases lifespan in age

-ad increases with age this if population increases so does ad

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2
Q

What are the 4 main facts about ad

A
  • occurs in 5%of the population and the most common neurodegenerative disease
  • 1:6 people over age 80
  • memory failure
  • poor navigational skills
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3
Q

What are the 2 main types of causes for ad?

A
  • sporadic the most common and no obvious heritable gene
  • genetics <10% of the population and genome wide association studies -familial

But also said that the environment can too influence vulnerable to genetics and developing ad

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4
Q

What is the first symptom of ad

A

failing memory which starts off in the hippocampus which makes sense because this area is involved in navigation and conscious memories

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5
Q

What are the clinical characteristics of ad

A

Memory
-failing memory for recent events and it is disproportionally worse than age related decline.

Other areas affected

  • deficits in spatial navigation
  • aggression and apathy
  • depression
  • change in personality
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6
Q

Fun facts about ad (6)

A

Fun facts about ad (6)

  • difference In post mortems of the Brian with ad and pd and the areas that are affected reflect the different symptoms that experienced
  • ad become more widespread in brain
  • initially the brain doesn’t look any different to the normal brain but the progressively gets worse
  • loss of temporal love hence match symptoms first experience like poor naviagation and memory
  • ad is hard to diagnose at first because primary symptoms are poor memory this think may be related to age related decline instead
  • forgetting gets worse, where individuals loose the ability to recognise family members
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7
Q

What isit not surprising that many symptoms are experienced in ad

A

Because degeneration occurs in temporal lobe and spreads to many other areas of the brain

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8
Q

Where does degeneration occur

A

Temporal lobe first

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9
Q

What happens during degeneration

A

Neuronal loss- caused by neurofibral tangles and amyloid plaques

Said neurons loss correlate with these plaques and tangles

Synapse loss-
Correlates with cognitive impairment
Affects cholinergic and glutaminergic synapse

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10
Q

What’s difference between pd and ad in degeneration

A

No dopamine neuronal loss hence why different symptoms are experienced

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11
Q

What are the 2 type of neurons and synapse affected

A

Cholinergic and glutaminergic

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12
Q

Why is arc important

A

Seen to be involved the capacity of memories

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13
Q

What happens if less glutamate and ache from synapse and neuronal loss

A

Less released into synapse less bind to PSn and it’s receptors so less capacity for memories and less likely to form recent memories via synaptic plasticity for ach and nmda receptors

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14
Q

Why are old memories lost

A

Degeneration kills neurons which hold the old memories via synaptic plasticity

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15
Q

What so important about app protein caused by certain genes that make us vulnerable to app

A

Genes contribute to vulnerability found via genome wide studies and said gene when mutated produces app protein that also mutated socauses amyloid plaques and same for tau and neurofibrial plaques

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16
Q

Where will plaques and tangles first appear

A

In the temporal lobe

17
Q

What causes plaques

A

Beta amyloid peptide from app protein which aggregate

18
Q

Whaat is glutamate for

A

Learning and memory e.g bind to nmda receptors for recent memory formation and synaptic plasticity

19
Q

What the 2 treatments for ad

A

Drug treatment
-increase cholinergic transmission via inhibitor so have more capacity for memories
Prolong ach in synapse by inhibiting acetycholinesterase

20
Q

What the problem with boosting choline

A

Not effective

  • and if was the importance of choline why isn’t smoking which increases the activity of neurotransmitter result in a decrease in ad

They work at ach receptors also

21
Q

What other treatment for ad

A

Targeting pathology

  • add antibodies to bind to amyloid to prevent it aggregating and making plaques
  • or add drug that break down plaques
  • no effective potentially because plaques not causing the degeneration

Or not effective because degeneration so far gone that adding drugs serve little purpose