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A - Neuroinfectious Diseases Non-infectious Neurodiseases > Parkinson and Alzheimer > Flashcards

Parkinson and Alzheimer Flashcards

1
Q

PD and AD are both examples of

A

primary neurodegenerative diseases

dementia disorders

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2
Q

primary vs secondary neurodegenerative diseases

A

primary - death intrinsic on cell, do not know how to stop cell death

secondary - response to something else (ex. polio, siphilus)

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3
Q

dementia disorders

A

serious loss of cognition - ability to think and rationalize your surroundings

Is acquired - chronic, progressive, is a syndrome (collection/spectrum of symptoms)

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4
Q

progressive neurodegenerative diseases

A

Progressive destruction of nerve cells → death

Elderly grew forgetful → senile dementia

Various types of dementia, some treatable

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5
Q

Rising evidence that many are a type of prion disease

A

Accumulation of protein “plaques”

Nerve cell necrosis

Gliosis → activation of astrocytes, microglia

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6
Q

Most common form of dementia

A

Alzheimer’s
Amyloidosis, tauopathy

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7
Q

Alzheimer’s First described in 1906 by

A

psychiatrist Alois Alzheimer

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8
Q

AD patient zero

A

51 year-old suffering from severe dementia

Described the symptoms and the pathological manifestations

Extracellular deposits of a “peculiar substance” → amyloids

Intracellular fibrillary bundles → tau tangles

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9
Q

In 1976 AD accepted to be the cause of most

A

senile dementias

was considered to be a rare form of early- onset AD - more autopises showed was more common

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10
Q

AD hypothesis was confirmed when

A

rare mutation were discovered in chromosome 21 (contains APP gene)→ explained incidence of dementia in Down syndrome (b/c have more of amaloid-b gene)

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11
Q

nodding syndrome

A
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12
Q

____ mutations have been linked to AD since

A

> 50 APP

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13
Q

AD incidence in US

A

5 % of adults > 65
30 – 40 % of adults > 85

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14
Q

Top cauzes of death in high vs low income countries

A

Disproportionally prevalent in “developed” world - US and EU

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15
Q

AD incidence groups

A

Woman almost 2X more likely
- Framingham study since 1948 → still ongoing

African American woman > 5X
- Possibly due to diabetes (a risk factor for AD)

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16
Q

____ seems to be protective (AD)

A

Education

brain activity? Or just socioeconomic status?

also potential reason for women more likely - 40s and 50s were not allowed to study (even more so african american women)

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17
Q

____ of AD patients start with ____

A

> 75 %
memory problems

early - miss place things, issue with short term memory - not issue with long term memory yet

Motor functions spared until very late in AD

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18
Q

As AD progresses symptoms

A

(MM AL) Language, Mood, Memory, Activities

Language becomes less fluid, comprehension declines - other cogantive functions decline

Mood changes common: mild depression and social withdrawal - avoid people because cannot remember them

Memory loss more pervasive, involving older memories

Severely interfere with normal activities, i.e. driving

Problems walking, eating, taking care of themselves → economic and psychological burden on caregivers

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19
Q

Capgras syndrome

A

think people replaced by identical impostors

similar to psychosis - trying to make justify things with ideas

20
Q

AD Onset to death

A

8 – 10 years

21
Q

types of dementia

A

cortical (AD)
or subcortical (PD)

22
Q

AD MRI

A

black spaces - cell death
white spaces - inflammation

key difference with prion disease (no inflammation)

23
Q

AD classic example of

A

cortical

Loss of the cerebral cortex

Cell necrosis

“Senile plaques” → amyloid-β
AD tangles → hyperphosphorylated tau protein

Immune reaction to plaques → damaging inflammation (chronic)

Impaired clearance of wastes (white build up on capilaries - should be removed but not)

24
Q

“Senile plaques”

A

→ amyloid-β

25
Q

AD tangles

A

→ hyperphosphorylated tau protein

26
Q

Cellular issues in AD

A

Neuronal transport system is disrupted by tau tangles
- Less neurotransmitters, and other components, are delivered to synapses

Axon destruction

Plaques act as catalysts - dissemination/spread of AD

Plaques elicits inflammatory response -Neuron killing

27
Q

AD treatments

A

There are 4 FDA approved drugs → none is a cure

3 of them are inhibitors of cholinesterase → increases neurotransmitter availability [problem - not take NT to synapse, help by inc NT levels at synapse]

NMDA receptor antagonist → NMDA involved in learning, also allows glutamate import → glutamate toxicity

(enzyme → inhibitor
receptor → antagonist)

(some treatment uses both types)

28
Q

AD Early diagnosis is key, but problematic because

A

finding volunteers at ever- earlier stages of disease - hard - difficult to research

Research targeting the clearance of plaques promising → learning from prion research! (monoclonal antibody)

29
Q

Second most common progressive neurodegnerative diease

A

PD

30
Q

PD Described in 1817 as

A

“Shaking Palsy”

31
Q

3 classical symptoms of PD

A

Tremors
abnormal posture and gait
reduced muscle strength

32
Q

PD cortical vs subcortical

A

subcortical dementia - degeneration of the “substantia nigra” (in brain stem) neurons that produce a black pigment (DA producing)

33
Q

PD is thought to be a consequence of

A

genetics and environment

Up to 25 % of patients have a relative affected as well

34
Q

Incidence of PD

A

PD more common in men than women Caucasians 3X more likely

35
Q

Typical onset of PD

A

> 65 years-old

very rare early onset cases - purely genetic cases (7 genes involved so far)

36
Q

_____ are the earliest symptoms of PD

A

Tremors
are autorecognized - recognized by patient - first one to notice

37
Q

Other symptoms of PD

A

(MMM O) Motion, mood, dementia(memory), olfaction

38
Q

PD is Very well studied

A

oldest movement disorders identified, but also many celebrities with PD (Muhammad Ali or Michael J. Fox)

39
Q

synucleinopathy

A

synucleinopathy - exhibit Lewy bodies

PD is one of many

role in PD unclear - seems to be involved in propagation/spread over brain

40
Q

PD diagnositic

A

levadopa - DA precursor -if take and helps confirms PD disgnosis

41
Q

α-synuclein in PD

A

Lewy bodies → aggregates of α-synuclein → late stages → dementia

42
Q

The main causative pathology in PD is

A

death of dopaminergic neurons

43
Q

What kills DA neurons in PD? Why just them? Why other neurons are spared?

A
44
Q

PD treatments

A
45
Q

Are plaques cause or consequence

A

A - Neuroinfectious Diseases Non-infectious Neurodiseases (5 decks)

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