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NBB Test 2 > Alzheimer's Disease > Flashcards

Alzheimer's Disease Flashcards

1
Q

Not a disease itself but rather a group of symptoms that may accompany certain diseases or conditions

A

Dementia

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2
Q

Irreversible when caused by disease or injury but may be reversible when caused by drugs, alcohol, hormone or vitamin imbalances, or depression

A

Dementia

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3
Q

Often begn in pre-senescence

-Have both genetic and sporadic forms

A

Dementia syndromes

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4
Q

Involve abnormal protein aggregation in neural tissue that disrupts neuronal function

A

Dementia syndromes

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5
Q

Caused by mutations in genes that either code for or affect the function of a protein

A

Genetic forms fo dementia

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6
Q

Characterized by the presence of neuritic plaques and tangles, as well as synaptic and neuronal loss due to apoptosis

A

Alzheimer’s Disease (AD)

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7
Q

The most common age-related degenerative dementia, accounting for about 2/3 of all cases

A

AD

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8
Q

Usually begins with the gradual failure of recent (episodic) memory–alertness and motor functions are spared

A

AD

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9
Q

A clinical feature of AD that can also be reported as decreased taste

A

Anosmia

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10
Q

A small percentage (~1%) have AD onset before age 60 (“pre-senile”). These typically are inherited, and are referred to as

A

Familial AD (FAD)

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11
Q

Neuritic plaques contain extracellular deposits of insoluble fibrils composed of polymers of

A

Amyloid β-protein (Aβ)

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12
Q

Exhibit dystrophic morphologies and tau tangles

A

Neurites

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13
Q

Axons and dendrite trajectories are disrupted by

A

Neuritic plaques

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14
Q

Gliosis and microglia induce

A

Oxidative stress/inflammation

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15
Q

Arises from the normal processing of a longer transmembrane protein, Amyloid Precursor Protein (APP)

A

Amyloid β-protein

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16
Q

What is the name of the enzyme that cleaves APP to creat beta amyloid proteins

A

BACE (Beta-site APP Cleavage Enzyme)

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17
Q

Functions as a cell surface receptor/cell signaling or migration

-Also cell adhesion and neurite outgrowth and synaptogenesis

A

Amylolid Precursor Protein (APP)

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18
Q

Post-mortem studies of AD patients have shown that neuritic plaques are composed primarily of the

A

42aa form of Aβ protein

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19
Q

Extracellular accumulation of insoluble Aβ-42 disrupts neuronal and synaptic function, leading to cell death, and is the causative factor for

A

AD

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20
Q

Amyloid plaques and neurofibrillary tangles form in mice over-expressing* mutant forms of

A

Human APP and Tau

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21
Q

Is present in extracellular plaques in transgenic mice that over-express both proteins (i.e., this form is more prone to aggregate)
Mouse

A

Aβ-42 but not Aβ-40

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22
Q

Adults with Down (Trisomy 21) develop early onset AD (~age 40). This is correlated to increased

A

APP gene dosage/Aβ-42 production

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23
Q

To date, the only mutations known to cause dominantly inherited AD result in an excessive production/deposition of

A

Aβ-42

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24
Q

Lead to abnormal processing and, most commonly, increased production of Aβ-42 peptide

A

Missense mutations within the APP gene

25
Q

These mutations account for <0.1% of the AD cases

A

APP missense mutations

26
Q

A673T substitution reduces formation of Aβ by

A

40%

27
Q

A 34kD glycoprotein that is involved in cholesterol and lipids transport and may normally be involved in cell membrane repair

A

ApoE

28
Q

Inheritance of which ApoE increases the risk of developing AD (by 3-15 fold),

-Although it is neither sufficient nor required for disease development

A

Inheritance of ApoE4

29
Q

Produces a protein that is less stable than the other alleles

A

ApoE4

30
Q

Impairs Aβ-42 clearance, promoting aggregation

-Promotes tau hyperphosphorylation

A

ApoE4

31
Q

Similar to ApoE4

-Regulates Aβ-42 aggregation, deposition

A

Clusterin/Apolipoprotein J

32
Q

Complement related protein that may play a role in Aβ-42 clearance

A

CR1

33
Q

Involved in endocytosis

-May regulate APP trafficking in cells

A

PICALM

34
Q

Part of the gamma-secretase protein complex that produces Aβ-42 from APP

A

Presenilin Proteins (PS1, PS2)

35
Q

Gain of Function Mutations in Presenilin Genes are Associated with

A

FAD

36
Q

Mice with mutations in PS1 (that likely increases its stability or activity) show accelerated

A

Amyloid deposits

37
Q

Reduction in plaque load by antibody immunotherapy in humans does not improve

A

Memory Function

38
Q

Bind to specific neuronal receptors, which can result in cell death

A

Aβ oligomers

39
Q

Aβ oligomers bind to specific neuronal receptors including:

A

PrPc, EphB2, Fcy-RIIb, and LilrB2

40
Q

Expressed in the immune system and by neurons on growth cones and synapses

A

LilrB2 (leukocyte immunoglobulin-like receptor B2)

41
Q

Activation of signaling with Aβ oligomers triggers

A

Actin cytoskeletal disruption and synaptic loss

42
Q

Transgenic AD mice (APP/PS1) also lacking the mouse ortholog (PirB) are protected against

A

Neuronal damage and memory deficits

43
Q

Contain intracellular deposits of hyperphosphorylated tau (microtubule-associated) protein

A

Neurofibrillary tangles

44
Q

Important structural elements in neurons that are involved in cell/axon integrity and transport

A

Microtubules

45
Q

Abnormal phosphorylation renders tau less soluble and more prone to form

-impairs axonal transport of cargo

A

Filamentous aggregates

46
Q

The gene encoding tau is not genetically linked to AD, but it is linked to

A

Frontotemporal dementia

47
Q

What are the serum levels of Aβ-42 and Tau that suggest a patient is more likely to develop AD?

A

Low [Aβ-42] and high [tau]

48
Q

Stages of AD involving the entorhial and hippocampal cortex

A

Stages I-II

49
Q

The main input into the hippocampus and is responsible for pre-processing (familiarity) input signals

A

Entorhinal cortex

50
Q

One of the first symptoms of AD is

A

Impaired sense of direction and object recognition

51
Q

Involves the adjoining high order association areas of the basal temporal neocortex

A

Stages III-IV

52
Q

Involves additional neocortical association areas, eventually extends into the primary areas of the neocortex

A

Stges V-VI

53
Q

Language and cognition are profoundly effected in stages

A

V-VI

54
Q

Current pharmaceutical treatment strategies involves which 2 types of drugs?

A

Acetylcholinesterase inhibitors and NMDA antagonists

55
Q

May protect the brain from glutamate excitotoxicity

A

NMDA antagonist (Namenda)

56
Q

Physical exercise (elevation of heart rate for at least 30 minutes several times a week) may currently be the most effective therapy to prevent or offset

A

AD

57
Q

Projection neurons that have long, un- or sparsely-myelinated axons appear to be particularly susceptible to

A

AD

58
Q

Areas of the brain that are the most severely affected with AD appear to be involved in

A

Processing

59
Q

This idea correlates with studies showing that education, which directs waking brain activity away from default-mode to task-specific brain networks, may delay

A

AD onset

NBB Test 2 (33 decks)

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