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Brain and behaviour 2 > PBL 5: I'm Losing My Mind > Flashcards

PBL 5: I'm Losing My Mind Flashcards

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The Brain flashcards
1
Q

Define dementia

A

Progressive neurodegenerative disease, characterised by deterioration of intellect, behaviour and personality. It comes as a consequence of disease affecting the cerebral cortex and hippocampus

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2
Q

What is a cholinesterase inhibitor?

A

AChE inhibitors prevent the breakdown of AChE

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3
Q

What are physical signs and symptoms of dementia?

A 
Tremor
Balance problems
Speech and swallowing difficulties
Wandering
Visual issue
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4
Q

What are behavioural and psychological S+S of dementia?

A 
Agitation
Short-term memory loss
Depression
Disorientation and confusion
Agitation
Aggression
Sleep disturbances
Mood swings
Psychosis
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5
Q

Risk factors of dementia?

A 
Age
Genetics
Downs syndrome
High cholesterol
Diabetes
Environment (trauma)
Depression
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6
Q

What classification of dementia is there?

A 
Alzheimer's disease
Vascular dementia
Mixed AD and vascular
Lewy body dementia
Frontal-temporal/Pick's disease
Immunologically mediated (HIV/AIDS)
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7
Q

What is the presentation of Alzheimer’s disease?

A

Pre-dementia -> early -> moderate -> late

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8
Q

What symptoms worsen in Alzheimer’s disease?

A

Memory deficits
Impaired judgement and thought collection
Mood changes
Unusual behaviour acts

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9
Q

What is Alzheimer’s characterised by?

A

Formation of senile neuritic plaques from aggregations of beta amyloid peptide

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10
Q

What else is presented in Alzheimer’s apart from senile neuritic plaques?

A

Neurofibrillary tangles which are deposits of hyperphosphorylated tau proteins

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11
Q

What happens to structurally in AD?

A

neuronal loss
cerebral atrophy
loss of cholinergic projections

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12
Q

What are Amyloid precursor protein?

A

Gene responsible for making transmembrane, which can be cleaved to make amyloid-beta peptides (39-43 AA) in length

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13
Q

What usually cleaves APP?

A

Alpha-secretase then gamma secretase

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14
Q

What happens in AD with APPs cleaving wise?

A

Cleaved by beta-secretase then gamma secretase

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15
Q

What happens to the APP pathway in AD producing?

A

Beta-amyloid peptides (usually 42AA long) which aggregate to form senile plaques

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16
Q

What is presence of beta-amyloid plaques due to

A

formation of oligomers from peptides

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17
Q

What is a characteristic of oligomers which causes what?

A

Toxic leading to neuronal cell death as they are failed to be cleared away

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18
Q

What is the function of microglia?

A

recognise misfolded proteins which triggers inflammatory response

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19
Q

What do cytokines do?

A

Cause oxidative stress which alters activity of kinase and phosphorylation

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20
Q

What happens after activity of kinase and phosphorylation is altered?

A

Phosphorylation of tau proteins

21
Q

What do tau proteins do?

A

Stabilise microtubules in brain

THEY ARE NOT USUALLY PHOSPHORYLATED

22
Q

What does phosphorylation of tau do?

A

Regulate its ability to bind to and stabilise the microtubules

23
Q

What happens when tau becomes hyperphosphorylated?

A

Detaches from microtubules

24
Q

What do hyperphosphorylated tau proteins form?

A

neurofibrillary tangles in cell bodies

25
Q

What do neurofibrillary tangles do?

A

Impair axonal transport processes -> neuronal death + synapse loss

26
Q

What are the subunits of gamma secretase?

A

PSEN 1

PSEN 2

27
Q

What is related to early onset AD?

A

APP mutations

PSEN 1/2 (mainly 1)

28
Q

Where is PSEN 1 coded for?1

A

chromosome 44

29
Q

Where is PSEN 2 coded for?

A

chromosome 1

30
Q

Where do APOE4 mutations occur?

A

chromosome 19

31
Q

Which gene has relations to late onset AD?

A

APOE4

32
Q

What is APOE4 responsible for?

A

Clearance of beta-amyloid peptides

33
Q

Where is APP coded for?

A

Chromosome 21

34
Q

What is the Ach pathway?

A

Cholinergic forebrain pathways degenerate in AD so inhibit the breakdown of Ach by Ach inhibitors to increase Ach levels

35
Q

How to diagnose AD?

A

History + clinical presentation

MRI, PET or CT scans to image cerebral cortex

36
Q

What CSF biomarkers in AD?

A

Tau protein levels raised

Beta amyloid levels reduced

37
Q

What blood tests results may occur in dementia?

A

B12 deficiency

hypothyroidism

38
Q

What brain imaging can occur in dementia?

A

Compare hippocampal/ temporal loss in AD compared to frontal-temporal loss in other forms

39
Q

What brain regions are affected in AD?

A

Hippocampus in temporal lobe

40
Q

What are two processes of cellular plasticity linked with learning and memory?

A

Long term potentiation and long term depression

41
Q

What transmission are LTP and LTD?

A

glutamatergic transmission

42
Q

What do LTP do?

A

LTP strengthen synapses based on recent activity

43
Q

What do beta-amyloid plaques do to LDP?

A

increases LDP

reduces LTP

44
Q

What drugs are given for cholinergic pathway?

A

Donepezil
Rivastigmine
Galantamine

45
Q

What management of AD can be used?

A

Beta amyloid vaccine
ACh inhibitor
Anti-glutamatergic agents

46
Q

Why give anti-glutamatergic agents?

A

AD is associated with slow form of excitotoxicity involving glutamate

47
Q

What is excitotoxicity caused by in AD?

A

Influx of Ca2+ causing oxidative stress

48
Q

What is a NMDA receptor antagonist?

A

Memantine

49
Q

What are non-pharmalogical treatments of AD?

A

Cognitive stimulation therapy
Music therapy
Counselling
Reminiscent therapy

Brain and behaviour 2 (27 decks)

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