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Neuro 3 > Dementia Pathology > Flashcards

Dementia Pathology Flashcards

1
Q

What is the most common cause of dementia?

A

Alzheimer’s disease

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2
Q

What is the second most common cause of dementia overall?

A

Vascular disease -multi-infarct dementia -congophilic angiopathy -Binswanger’s disease

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3
Q

What is the second most common neurodegenerative cause of dementia?

A

LBD = Lewy’s Body Disease

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4
Q

Describe neuritic plaques

A

-amyloid beta peptide accumulations in the extracellular space

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5
Q

Describe neurofibrillary tangles

A

Accumulation of hyperphosphorylated tau protein that cause neuronal dysfunction and eventually neuronal death

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6
Q

What is congophilic angiopathy?

A

A-beta deposition in the walls of blood vessels in the CNS

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7
Q

Describe three changes in the gross anatomy of the brain that occur in Alzheimer’s disease progression

A

1) shrinkage of the cerebral cortex
2) shrinkage of the hippocampus (specifically loss of cholinergic pathways)
3) enlargement of ventricles (secondary to decrease in brain matter volume)

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8
Q

Define hydrocephalus ex vacuo

A

Enlargement of the cerebral ventricles or subarachnoid space

-usually due to brain matter atrophy (not increased CSF pressure like hydrocephalus)

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9
Q

What is tau protein’s normal function in the body?

A

Stabilizes microtubule formation in axons to maintain structure of the neuron

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10
Q

What happens to Tau protein in Alzheimer’s disease that contribues to the pathology?

A

-Tau protein gets phosphorylated, which changes its conformation and therefore its ability to perform properly

=> microtubules dissasemble which impairs axonal transport

-also hyperphosphorylated aggregates to form oligomers and neurofibrillary tangles that are toxic to neurons

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11
Q

What are pick bodies?

A

Histological/pathological finding of Alzheimer’s disease

  • pick bodies = spherical aggregates of Tau proteins in neurons
  • visible via silver stain
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12
Q

How long before onset of dementia symptoms do A-beta accumulations begin?

A

About 20 years before onset of dementia

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13
Q

Which start to accumulate first: A-beta or tau protein?

A

A-beta comes first

  • A-beta starts accumulating about 20 years before onset
  • Tau proteins start accumulating about 10 years before onset
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14
Q

Name two diseases besides AD that have tau-positive filamentous accumulations

A
  • Down’s syndrome
  • Fronto-temporal dementia
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15
Q

What is a presenilin mutation associated with?

A

-presenilin is an amyloid precursor protein

=> prensilin mutation => early onset AD due to earlier neuritic plaque acumulation

-familial/early onset Alzheimer’s

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16
Q

What percent of AD cases are familial vs. sporadic?

A

5% familial (PS1, PS2, APP mutations), onset < 65 yoa

95% sporadic, onset > 65 yoa

17
Q

What are some environmental risk factors for AD?

A
  • age, HTN, hypercholesterolemia, stroke, diabetes
  • head trauma
18
Q

What is the strongest genetic risk factor for AD?

A

ApoE genotype

-E4/E4 homozygotes have an 8-10x increased risk of developing AD

19
Q

What is the mechanism of ApoE’s role in AD?

A

ApoE localizes w/ Abeta plaques

  • ApoE binding helps stsabilize Abeta polymers
  • apolipoprotein E4 promotes Abeta aggregation and impedes brain clearance
20
Q

What are two possible immunotherapeutic options against AD?

A

Monoclonal antibodies against Tau protein and Abeta

21
Q

How can Binswanger’s Disease be prevented?

A

By managing HTN and DM thoughout the lifespan in attempt to prevent atherosclerotic build up in the blood vessels of the CNS

22
Q

What is Binswanger’s disease?

A

Vascular dementia

= subcortical leukoencephalopathy

-arterioles get infiltreated w/ lipid (so associated w/ HTN and/or DM) which causes loss of perfusion to surrounding neurons which causes demyelination

23
Q

Binswanger’s Disease

(a) Arteriole walls
(b) Perivascular space
(c) Location of demyelination
(d) Cerebral ventricle size

A

Binswanger’s Disease

(a) Thickened arteriole walls due to lipid infiltration
(b) Widened perivascular space
(c) Perivascular demyelination resulting from vessel pathology
(d) Enlarged ventricles due to shrinkage and softening of white matter

24
Q

What is a possible link btwn AD and vascular dementia?

A

Abeta deposition is toxic to endothelial cells => Abeta dposition can predispose to hemorrhage and ischemia (contributing to vascular dementia)

25
Q

What is Lewy Body dementia?

A

Form of dementia closely associated w/ Parkinson’s Disease characterized by presence of Lewy bodies

26
Q

How to clinically differentiate AD and Lewy Body dementia

A
  • AD often presents w/ short term memory loss
  • LBD diagnosed by dementia + marked fluctations in attention/alertness + parkinsonism. Visual hallucinations, delusions may be present
27
Q

What pathology stains positive for alpha-synuclein proteins?

A

Lewy Bodies

-characteristic of Lewy Body dementia (dementia associated w/ Parkinsons)

28
Q

What is another name for Brainstem predominant Lewy Body dementia?

A

Parkinson’s disease

29
Q

What is fronto-temporal dementia?

A

The clinical presentation of frontotemporal lobe degeneration

-most commonly presents w/ behavioral changes

30
Q

FTD (frontotemporal dementia) vs. AD (Alzheimer’s)

(a) genetic component
(b) age of onset
(c) most common presentation

A

(a) FTD has a 20-30% genetic component while AD has only 5% of cases due to genetics
(b) FTD has peak onset from 55-65 yoa (rarely seen after age 75) while incidence of AD continues to increase w/ age
- same incidence in younger ages, then AD takes over
(c) FTD most commonly presents w/ behavioral changes while AD presents w/ short-term memory loss

31
Q

What are the two main presentations of FTD?

A
  • gradual and progressive change in both behavior and language dysfunction
  • doesnt present w/ memory dysfunction like AD does
32
Q

What are TDP-43 inclusions an indication of?

A

FTD = frontotemporal dementia

-50% of FTD’s have inclusions of FDP-43, 40% of FTD’s have tau inclusions

33
Q

Flame shaped inclusions

A

Indicative of TDP-43 or ubiquitin inclusions of FTD (frontotemporal dementia)

34
Q

Distinguish AD and FTD on PET scan

A

AD on PET scan has more diffuse hypometabolism, while FTD shows hypometabolism specifically in the frontal and temporal lobes

35
Q

What histological finding is characteristic of prion disease?

A

Spongiform Change

36
Q

General pathogenesis of many neurodegenerative diseases

A

Normal proteins accumulating in a beta-sheet = toxic conformation

37
Q

Describe prion disease

A
  • group of neurodegenerative conformational disorders
  • conformation change in PrpC –> PrPsc
  • PrpSC has a high secondary beta-pleated sheet structure which has a tendency to aggregate and form amyloid fibers (which are toxic)
38
Q

What is the most common human prionosis?

A

Jakob-Creutzfeld DIsease

  • rapid progressive cognitive dysfunction (death < 1 year from onset)
  • CSF has elevations in tau protein and a protein reflecting rapid neuronal death
39
Q

H & E findings of Jakob-Creutzfeld-disease

A

Spongiform change (human prion disease)

Neuro 3 (7 decks)

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