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Term 5: Neuro > 6/3- Neuropathology of Dementia > Flashcards

6/3- Neuropathology of Dementia Flashcards

1
Q

Key feature (anatomical) of dementia?

A

Cortical degeneration

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2
Q

Causes of cortical degeneration?

A
  • Alzheimer’s dz
  • Pick’s dz (frontotemporal dementia)
  • Lewy body dementia

These are the 3 MCCs of neurodegenerative dementia (each have varied initial symptoms)

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3
Q

What does this show?

A

Cortical atrophy

(Left side shows caudate atrophy and hydrocephalus ex vacuo of Alzheimer’s dz?)

(Right side shows frontotemporal degeneration/Pick’s disease; selective in frontal and temporal regions)

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4
Q

2 categories of dz within Alzheimer’s?

A

Classical

Variant

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5
Q

2 categories of disease within Non-Alzheimer’s neurodegenerative diseases with dementia?

A

Tauopathies (PSP):

  • FTD complex/Pick’s dz

Synucleinopathies (PD, LBD):

  • Lewy Body Complex
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6
Q

What is seen microbiologically in Alzheimer’s dz?

A
  • Beta-amyloid (extracellular) + Tau (intracellular)
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7
Q

What is seen microbiologically in Pick’s dz/FTLD?

A
  • Tauopathy (pure)
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8
Q

seen microbiologically in Lewy Body Dementia (LBD)?

A
  • Alpha synuclein
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9
Q

Where does atrophy start in Alzheimer’s?

A

Starts in amygdala, hippocampus, and temporal lobe

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10
Q

Neuronal changes in Alzheimer’s?

A
  • Loss of cortical cholinergic innervation

(Central) cholinesterase inhibitors now in clinical use in mild-moderate cases

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11
Q

Characteristics of Alzheimer’s dz (symptoms)?

A
  • MEMORY DISTURBANCES
  • Starts with short-term memory
  • Onset may be subtle
  • Early onset cases are typically genetic
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12
Q

What anatomical features are seen grossly with Alzheimer’s?

A

Cortical atrophy and hydrocephalus ex vacuo

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13
Q

Histological features of Alzheimer’s dz?

A
  • Neuritic plaques- EXTRAcellular
  • Neurofibrillary trangles- INTRAcellular
  • Amyloid deposition in mature neuritic plaques and in the walls of cortical and leptomeningeal blood vessels
  • Many people believe that the plaques (beta-amyloid) are the initiating event and the tangles (hyperphosphorylated tau) are 2ndary
  • AD therefore is a beta-amyloidopathy
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14
Q

What is this?

A

Plaques and tangle seen in Alzheimer’s dz

  • Silver stain binding proteins rich in B-sheets and fibrillogenesis Seen center left is a plaque (extracellular)
  • Black structures are axons adjacent to deposition of B-amyloid; stuff like tau begins to accumulate within the processes
  • Most of the plaque is comprised of B-amyloid with neuroprocesses with accumulations of tau

Seen center right is a process with accumulation of tau (tangle?)

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15
Q

CERAD plaque estimation in Alzheimer’s dz (picture)

A

Few, moderate, or many

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16
Q

What is this?

A

Neurofibrillary tangles in Alzheimer’s dz (deposition of tau)

  • When tau is deposited in this way, it becomes hyperphosphorylated
17
Q

Plaque staging or counting has a ____ (good/poor) correlation with dementia. Tangle staging has a ___ (good/poor) correlation with dementia.

A

Plaque staging or counting has a poor correlation with dementia (HOW MANY PLAQUES)

Tangle staging has a good correlation with dementia (WHERE ARE THE TANGLES)

18
Q

Progression of Alzheimer dz (main steps)?

A
  • Pre-symptomatic
  • Mild cognitive impairment (MCI)
  • Alzheimer’s dz
19
Q

Progression of Alzheimer’s: Pre-symptomatic?

A

The pt has no cognitive impairment.

There is growing evidence that EC beta-amyloid is accumulating and tangles are beginning to form, esp in the hippocampus and adjacent temporal cortex

20
Q

Progression of Alzheimer’s: Mild cognitive impairment (MCI)?

A

The pt has mild deterioration of memory and cognitive function that worries the patient but which does not interfere with daily living

21
Q

Progression of Alzheimer’s: Alzheimer’s dz?

A

These individuals are frankly demented on clinical examination, neuropsychological evaluation and there is impairment of activities of daily living

22
Q

T/F: Alzheimer’s plaques can grow overnight

A

True

Study with mice has shown that they can grow significantly overnight

23
Q

Timeline of plaque development/growth in Alzheimer’s?

A

Plaques form in a day; macrophages/microglia react within a couple days; neurotic processes form within days

- Day 1: microplaque

- Day 2: distended neurites, amyloid-B-oligomer, astroglia and microglia first appear

- Day 3: dystrophic neurites

- Day 7: mature plaque

24
Q

How many people with MCI will go on to develop Alzheimer’s?

A

Roughly 1/2

25
Q

What is this?

A

Amyloid angiopathy in Alzheimer’s dz

  • Beta amyloid in vascular walls (typically cleared in blood, but if excessive accumulation in EC space, can build up in vessel wall -> fragility and IC hemorrhaging)
26
Q

What is Pick’s disease? Key clinical features?

A

Frontotemporal dementia

  • Uncommon severe dementing dz Symptoms
  • FRONTAL DISINHIBITION
  • (rare cases of new artistic/musical abilities)
27
Q

Micro anatomical features of Pick’s disease?

A

Micro:

  • Neuronal loss and gliosis
  • Ballooned neurons
  • NO plaques, tangles, or granulovacuolar
  • Faintly basophilic intraneuronal cytoplasmic inclusions (Pick bodies) immunoreactive for tau

Pick’s is a pure TAUOPATHY

28
Q

Gross anatomical features of Pick’s disease?

A

Gross:

  • Marked temporal and frontal atrophy
  • “Knife edge” gyri
  • Sparing of post 2/3 of superior temporal gyrus, parietal lobes, and precentral (motor) gyrus
29
Q

What is this?

A

Cortical atrophy seen in Pick’s disease (Frontotemporal Atrophy

) - so thin gyri that they look like “knife edge”

30
Q

What is this?

A

Pick bodies in Pick’s dz

31
Q

What is this?

A

Tau inclusions: Globose tangles in PSP

  • Silver stain
32
Q

What is this?

A

Tau inclusions: Pick bodies in Pick’s dz

  • Silver stain; Pick bodies are the larger blots while nuclei are smaller
33
Q

What is this?

A

Neuronal loss, gliosis, rarefaction in Pick’s dz

  • Rarefied = not many neurons; a lot of open space
  • Notice: no plaques (unlike AD)
34
Q

What is seen micro in Lewy Body Dz?

A
  • Subtle eosinophilic cytoplasmic inclusions in cortical neurons (Lewy bodies)
  • Difficult to identify on H&E; immunopositive with alpha-synuclein
35
Q

What is the most common cause of dementia? 2nd most common cause?

A

1st: Alzheimer’s disease
2nd: Lewy Body disease

36
Q

Clincical features of Lewy Body disease?

A
  • Fluctuating cognitive features (starkly different from day to day!)
  • Visual hallucinations (often well-formed, cartoon-like; pt is aware that they are hallucinating)
  • Extrapyramidal features may occur (e.g. some features of Parkinsonism)
37
Q

What is this?

A

UL: Parkinson’s disease (loss of SN)

UR: Lewy bodies in pigmented neurons with central core and halo

LL: Lewy body

LR: Cortical Lewy Bodies

(PD and LBD are synucleinopathies)

38
Q

What is this?

A

Cortical Lewy Bodies

  • a-synuclein

(Parkinson’s dz and Lewy body dementia are synucleinopathies)

39
Q

Pharmacological approaches?

A

Central cholinesterase drugs

  • Donepezil
  • Rivastigmine
  • Galanthamine

Glutaminergic neurotransmission modulators (use any place there’ degeneration and a lot of glutamate buildup)

  • Riluzole (for ALS)
  • Memantine (for Alzheimer’s)

Parkinsonism Sx (in LBD) may be treatable with DA, but cost may exceed therapeutic benefit

Term 5: Neuro (24 decks)

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