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MBD/MI (Wothaya) > Neurodegenerative Diseases > Flashcards

Neurodegenerative Diseases Flashcards

1
Q

What is neurodegeneration?

A

The progressive loss of neurons

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2
Q

What part of the nervous system do neurodegenerative diseases affect?

A

CNS, PNS or both

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3
Q

When do neurodegenerative diseases begin?

A

At any time

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4
Q

What does an earlier age of onset mean?

A

Greater genetic contribution

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5
Q

What does a later age of onset mean?

A

More likely sporadic disease

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6
Q

What is the common pattern of most neurodegenerative diseases?

A

Molecular impairment in the cell
Decreased transmission at synapse
Dying back of neurites
Cell death

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7
Q

What do neurodegenerative diseases frequently involve?

A

Protein aggregation
Lysosomal dysfunction
Mitochondrial dysfunction
Associated inflammation via activation of glia

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8
Q

What are some of the clinical/ research issues in neurodegenerative diseases?

A

Rarely manifest obvious symptoms until pathology is severe
Study of affected tissue is tricky until after death
Remains incurable

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9
Q

What is the most common neurodegenerative disease?

A

Alzheimers

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10
Q

When is normal onset of alzheimers?

A

> 65 yrs

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11
Q

What proportion of alzheimers are early onset and when is this?

A

10%

30s onwards

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12
Q

What proportion of people have alzheimers aged 85+?

A

50%

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13
Q

What characterises dementia?

A

Decline in memory and other cognitive functions that impair quality of life

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14
Q

What is ‘normal ageing’?

A

Gradual decline in normal cognition, gradual changes in personality

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15
Q

What are some pathological hallmarks of dementia?

A

Brain shrinkage

Proteinopathies

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16
Q

What types of proteinopathies are present in dementia?

A

Amyloid plaques

Neurofibrillary tangles

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17
Q

What are amyloid plaques enriched in?

A

A beta peptides

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18
Q

What is another name for neurofibrillary tangles?

A

Paired helical filaments

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19
Q

What is A beta?

A

Peptide cleaved from amyloid beta precursor protein which accumulates to form a plaque

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20
Q

What are neurofibrillary tangles?

A

Intracellular protein aggregates that are enriched in Tau protein

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21
Q

What is the amyloid hypothesis?

A

A beta and/or amyloid plaques are the cause of alzheimers

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22
Q

What are the three protein mutations involved in the amyloid hypothesis?

A

APP, PSEN1 and PSEN2

23
Q

What are PSEN1 and 2 both components of?

A

Gamma secretase

24
Q

What does tau normally do?

A

Binds microtubules in axons

25
Q

What does displacement of hyperphosphorylated tau cause?

A

Tangles and destabalised molecules

26
Q

What are the three main roles of microtubules in post-mitotic cells?

A

Structure/ shape of a cell
Positioning of organelles
Motorways for transporting vesicular contents

27
Q

Why is the tau hypothesis plausible?

A

In typical late onset alzheimers, neurofibrillary tangles are seen before amyloid plaques and well correlated with cell death and progression

28
Q

What does the tau hypothesis suggest?

A

Tau is upstream of A beta

29
Q

What are some other risk factors for alzheimers?

A 
Down syndrome
Gender (women) 
High BP, CVD and diabetes
Low education
Head injury
Smoking and drinking
Small genetic risk contribution
30
Q

What is the second most common neurodegenerative disease?

A

Parkinsons

31
Q

What is the average age of parkinsons disease onset?

A

60-65 yrs

32
Q

What are the motor symptoms in parkinsons?

A

Resting tremor
Bradykinesia
Rigidity
Postural instability

33
Q

What are the non-motor symptoms of parkinsons?

A 
Depression and anxiety 
Loss of smell
Sleep disorders
Constipation
Dementia
34
Q

What are some of the pathological hallmarks of parkinsons?

A

Loss of dopaminergic neurons of the substantia nigra

Proteinopathies (Lewy bodies)

35
Q

What are lewy bodies?

A

Intracellular protein aggregates enriched in alpha-synuclein protein

36
Q

Are lewy bodies pathogenic?

A

No

37
Q

What are the three rough categories for causes of parkinsons?

A

Early onset autosomal recessive mitochondrial conditions
Late onset autosomal dominant
Mutations that cause ‘parkinsons plus’ conditions

38
Q

What causes Early onset autosomal recessive mitochondrial conditions?

A

Loss of function mutations in PINK1 and parkin cause decreased mitophagy

39
Q

What does autosomal dominant parkinsons cause?

A

Alpha synuclein gene amplification
LRRK2 gain of function
VPS35 gain of function
GBA loss of function

40
Q

What does GBA encode?

A

GCas - a lysosomal enzyme

41
Q

Where is alpha synuclein degraded?

A

In the lysosome

42
Q

What is the pathogenic feed-forward loop?

A

Alpha-synuclein inhibits the transport of GCas into the lysosome, which decreases lysosomal function

43
Q

How much of parkinsons is genetic?

A

30%

44
Q

What are the risk factors for parkinsons?

A 
Gender (men) 
Red hair
Head injury
Not smoking/consuming caffeine
Herbicides, pesticides, insecticides
Exposure to metals
General anaesthesia
45
Q

What is neuroinflammation?

A

Activation of the immune system within the nervous system

46
Q

What are the features of reactive microglia?

A

Amoeboid shape
More motile
Production of cytokines
Eventually phagocytic

47
Q

How does neuroinflammation cause neurodegeneration?

A

Neurotoxic insult (causing neuronal damage/death)
Release of microglial activators
Reactive microglia release neurotoxic factors like IL-1B, TNF-alpha and prostaglandins

48
Q

What can reactive microglia cause?

A

Protection or damage of neurons

49
Q

How are reactive microglia protective of neurons?

A

Anti-inflammatory cytokine release -> contributes to normal removal of unhealthy cells

50
Q

How can reactive microglia be damaging to neurons?

A

Proinflammatory cytokine release in response to pathogens

51
Q

What does ageing induce a shift towards?

A

Production of damaging reactive microglia due to changes in microglia expression

52
Q

What can microglia be activated by?

A

External triggers (Abeta, environmental toxins and pathogens)

53
Q

What precedes lewy body pathology in brain?

A

Lewy body pathology in the gut

54
Q

What are some effects of ageing?

A

Shortening of telomeres in adults
Increased reactive oxygen species
Changes in gene expression (decreased wnt beta catenin pathway in adult brain)

MBD/MI (Wothaya) (57 decks)

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