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1.Alzheimer Disease > J.Neuropathol.Exp.Neurol.2012Review > Flashcards

J.Neuropathol.Exp.Neurol.2012Review Flashcards

1
Q

Although the severity AB plaques may play a key role in AD pathogenesis, the severity of cognitive impairment correlates best with what?

A

The burden of neocortical neurofibrillary tangles (NFTs)

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2
Q

What is required for a definitive diagnosis of AD?

A

Autopsy

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3
Q

Neurofibrillary pathology comprises what? (5)

A

-Aberrant
-Partly Soluble
-Protease-Resistant
-Hyperphosphorylated
TAU AGGREGATES

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4
Q

Neurofibrillary pathology by Electron Microscopy shows what?

A

Paired helical filaments

  • Inside various cellular components OR
  • Extracellular after death of the parent cell
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5
Q

Neurofibrillary tangles (NFTs) describes what?

A

Neurofibrillary pathology found in cell bodies

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6
Q

What is a pretangle?

A

Contains abnormal hyperphosphorylated TAU in nonfibrillar (partially soluble) and non argyrophilic forms.

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7
Q

T/F: Pretangles are capable of developing into NFTs.

A

True

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8
Q

What are amyloid plaques that contain the Amyloid Beta peptide (ABPs)?

A
  • Extracellular
  • Spherical (roughly) structures
  • Contain AB peptide and other material
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9
Q

ABPs can be detected histologically with what special stains? (3)

A
  • Congo Red
  • Silver Stains
  • Thioflavin-like Molecules
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10
Q

Diffuse ABPs may be visualized using what?

A

Silver stains and anti-AB immunostains

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11
Q

What are Neuritic AB plaques (NPs)?

A

-ABPs that are invested by swollen, degenerating neurites and glial cell processes

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12
Q

In NPs, what do the swollen neurites contain?

A

Filamentous TAU protein aggregates

-Structurally identical to the inclusions with the NFT

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13
Q

The density of NPs is graded according to what?

A

Consortium to Establish A Registry for Alzheimer’s Disease (CERAD) criteria

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14
Q

By definition, what do diffuse plaques lack?

A

Dystrophic tau-immunoreactive neurites

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15
Q

Braak stages refer to what?

A

Hypothetically predictable progression of NFT-type pathologic features in the brain during the course of Alzheimer disease.

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16
Q

Braak stages:

-(I-III)

A

Early stages

-Medial Temporal lobe structures ONLY

17
Q

Braak stages:

-(IV-VI)

A

Later stages

-Progressively affect the neocortex

18
Q

Medial Temporal Lobe Structures (MTLs) comprise what structures? (4)

A
  • Amygdala
  • Entorhinal Cortex*
  • Cornu Ammonis (CA) fields*
  • Subiculum of the Hippocampus*

*Allocortical structures

19
Q

MTLs play important role in what?

A

Consolidating short-term memory

20
Q

Hippocampal pathology is ubiquitous in AD patients but is not relevant for clinicopathologic correlation due to what?

A

Strong “floor-and-ceiling” effects

21
Q

What is the areas of cerebral cortex outside of allocortical areas refered to as?

A

Isocortex/Neocortex

22
Q

What is the function of the neocortical areas?

A

Higher order function

  • Judgement
  • Executive function
23
Q

T/F: The distinction between the MTL areas and neocortical areas is important in comprehending the predictable, but nonlinear, progression of pathology in AD.

A

True

24
Q

What are the neuropathologic hallmarks of AD?

A
  • Neurofibrillary tangles (NFTs; including pretangles)
  • Amyloid Beta plaques (ABPs; including diffuse and neuritic plaques*)

*also referred to as “senile plaques”

25
Q

What are some additional (not pathognomic) changes seen in brains of AD patients? (8)

A
  • Amyloid angiopathy
  • Age-related brain atrophy
  • Synaptic pathology
  • White matter rarefaction
  • Granulovaculolar degeneration
  • Neuron loss
  • TDP-43 proteinopathy
  • Neuroinflammation
26
Q

T/F: Neurofibrillary tangles are not specific for AD.

A

True

“NFTs are found in both controls and dements in the hippocampus, but elsewhere in the cortex was only severe or widespread in the dements…” -Tomlinson et.al (1970)

27
Q

What are some other conditions were NFTs are found? (9)

*What does this suggest?

A
  • Frontotemporal Lobar Degeneration with Tauopathy (FTLD-MAPT)
  • Focal Cortical Dysplasia
  • Myotonic Dystrophy
  • Prion Diseases
  • Metabolic/Storage Diseases
  • Brain Tumors (some)
  • Chronic Traumatic Encephalopathy
  • Viral Encephalitis
  • Other Brain diseases

*NFTs are, at least under some conditions, a secondary response to injury.

28
Q

Neurofibrillary degeneration restricted to what anatomical locations are typically subclinical?

A

Subcortical sites

29
Q

Where are Amyloid Beta plaques located?

A

Extracellular

30
Q

T/F: ABPs are found in a high proportion of ALL elderly persons but are not universal.

A

True

31
Q

What ABP subtype is more likely to be associated with cognitive impairment?
-What is the other subtype?

A 
Neuritic plaques (NPs)
-"diffuse plaques"
32
Q

What are Neuritic Plaques?

A

ABPs surrounded by degenerating axons and dendrites
-Contain hyperphosphorylated TAU aggregates

*Hallmark of the current diagnostic criteria for AD

33
Q

What are the High-Penetrance AD genetic risk alleles? (4)

A
  • APOE e4 allele
  • Trisomy 21
  • APP mutations/duplications
  • PSEN1/PSEN2 mutations
34
Q

What are the high-penetrance AD genetic risk alleles associated with?

A

Increased AB deposition and increased formation of putative toxic AB peptide species

35
Q

Genetic factors confer approximately __% of an individuals risk for AD.

A

70%

36
Q

Dense and extensive neocortical ___ are very consistently associated with dementia and thus, according to new diagnostic criteria, are required to constitue high burden of AD neuropathologic change.

A

NFTs

37
Q

What are the effects of anti-AB immunotherapy in patients with mid- to late-stage AD?

A
  • Partially cleared ABPs
  • No effect on NFT formation
  • Little effect on disease course
38
Q

In most community-based autopsy series, non-AD tauopathies constitute approximately ___% of dementia cases.

A

1%

39
Q

What are the Non-AD Tauopathies? (6)

A
  • FTLD-MAPT
  • Progressive Supranuclear Palsy
  • Corticobasal Degeneration
  • Pick Disease
  • Argyrophilic Grain Disease
  • “Tangle-Only Dementia”

1.Alzheimer Disease (1 decks)

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