Parkinson and Alzheimer Flashcards

(45 cards)

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
AD tangles
→ hyperphosphorylated tau protein
26
Cellular issues in AD
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
AD treatments
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
AD Early diagnosis is key, but problematic because
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
Second most common progressive neurodegnerative diease
PD
30
PD Described in 1817 as
"Shaking Palsy”
31
3 classical symptoms of PD
Tremors abnormal posture and gait reduced muscle strength
32
PD cortical vs subcortical
subcortical dementia - degeneration of the “substantia nigra” (in brain stem) neurons that produce a black pigment (DA producing)
33
PD is thought to be a consequence of
genetics and environment Up to 25 % of patients have a relative affected as well
34
Incidence of PD
PD more common in men than women Caucasians 3X more likely
35
Typical onset of PD
> 65 years-old very rare early onset cases - purely genetic cases (7 genes involved so far)
36
_____ are the earliest symptoms of PD
Tremors are autorecognized - recognized by patient - first one to notice
37
Other symptoms of PD
(MMM O) Motion, mood, dementia(memory), olfaction
38
PD is Very well studied
oldest movement disorders identified, but also many celebrities with PD (Muhammad Ali or Michael J. Fox)
39
synucleinopathy
synucleinopathy - exhibit Lewy bodies PD is one of many role in PD unclear - seems to be involved in propagation/spread over brain
40
PD diagnositic
levadopa - DA precursor -if take and helps confirms PD disgnosis
41
α-synuclein in PD
Lewy bodies → aggregates of α-synuclein → late stages → dementia
42
The main causative pathology in PD is
death of dopaminergic neurons
43
What kills DA neurons in PD? Why just them? Why other neurons are spared?
44
PD treatments
45
Are plaques cause or consequence