Neuropathology Flashcards

1
Q

What is seen in the gross brain tissue of AD brains?

A

Dystrophy- wider sulci- atrophy

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2
Q

With the development of silver staining, what was allowed to be visualised in AD brains

A

Amyloid beta plaques and neurofibrillary tangles

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3
Q

Are amyloid plaques present in all AD brains and are all brains with amyloid plaques in AD patients?

A

no

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4
Q

List 5 risk factors for dementia

A

5 of:
age, small brain, Alzheimer’s lesions (Amyloid plaques and NFTs), vascular pathologies, hippocampal atrophy, cerebral amyloid angiopathy, Lewy bodies

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5
Q

what is the key difference seen in the brains of Parkinson’s disease patients ?

A

loss of dopamine neurons from Substantia Nigra

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6
Q

what is used to treat PD?

A

dopamine replacement therapy

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7
Q

what are the issues with dopamine replacement therapy?

A

doesn’t work long term
many side affects

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8
Q

name the 2 genes mentioned in lecture associated with PD

A

PINK1 and TIGARB

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9
Q

what have PINK1 Knockout studies shown?

A

links to mitochondrial deficiency, leading to dopaminergic neuronal loss in PD

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10
Q

what has upregulation of TIGAR protein in fish models shown?

A

dopaminergic apoptosis

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11
Q

which gene/protein has also been associated with Lewy bodies in SN dopaminergic neurons?

A

TIGARB

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12
Q

What typical microscopic feature is seen in cells of MND patients?

A

ubiquitylated inclusions

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13
Q

which gene have lectures mentioned to be closely linked to MND

A

TDP-43

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14
Q

Where has TDP-43 been seen in MND brains?

A

within ubiquylated inclusions in cells

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15
Q

what is TDP-43?

A

RNA processing gene/protein

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16
Q

what other disorder is closely linked to MND with similar pathology?

A

chronic traumatic encephalopathy

17
Q

what causes chronic traumatic encephalopathy?

A

blows to head- sports

18
Q

which protein has been seen in both CTE and MND patients?

A

TDP-43

19
Q

What genetic differences were mentioned to be seen in gliomas?

A

loss of 1p and 19q

20
Q

do brain tumours typically have an older or younger age onset than other tumours?

A

younger

21
Q

what kind of damage is closely associated with glutamatergic signalling?

A

excitotoxicity

22
Q

what does excitotoxicity do cellularly at the synapse?

A

causes an excessive calcium influx

23
Q

what 3 damaging effects can this calcium influx caused by excitotoxicity have?

A

mitotoxicity
induces apoptosis
induce nitrous oxide synthase

24
Q

how does mitotoxicity happen?

A

mitochondria buffer calcium, however, when overloaded can generate ROS’

25
Q

how is apoptosis induced in excitotoxity?

A

caspase-3 induction through excessive calcium

26
Q

what does nitrous oxide induction do?

A

generates nitrous oxide species that alter mitochondrial permeability leading to solute overload and mitochondrial swelling

27
Q

if a nerve conduction study shows a response that is too small, what does this generally mean?

A

neuronal loss

28
Q

if a nerve conduction study shows a response that is too slow, what does this generally mean?

A

myelin loss

29
Q

if electromyography studies show a response with an increased amplitude and length, what does this mean?

A

there has been denervation and remaining nerves have taken over the space, hence more nerves causing an increased response.

30
Q

if electromyography studies show a response with reduced amplitude and length, what does this mean?

A

muscle disintegration

31
Q

Which type of communication is effected in myasthenia gravis?

A

nerve and muscle (neuromuscular junction)

32
Q
A