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EXP NEURO > Neurodegenerative disorders > Flashcards

Neurodegenerative disorders Flashcards

1
Q

prevalence of alzheimers disease (AD):

A
  • worldwide cost of US $818 billion

- by 2018, cost above US$ trillion

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2
Q

AD treatments: usually agonist/antagonist and con

A
  • cholinergic agonist
  • NMDA antagonist
  • only symptomatic (doesn’t reverse slow course of disease)
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3
Q

AD: clinical definition

A
  • presence of early and sig episodic memory impairment (isolated/associated) w other cognitive or behavioural changes that are suggestive of mild cognitive impairment or of a dementia syndrome incl etc..
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4
Q

AD: 2 classifications

A
  • early onset AD (EOAD) <65yrs

- late onset AD (LOAD) >65yrs

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5
Q

AD: list 3 specific classifications

A
  • sporadic EOAD
  • familial EAOD
  • autosomal dominant AD
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6
Q

AD: affected brain regions (3)

A
  • damaged cortex (thinking, memory, planning)
  • shrinkage: esp hippocampus (formation of new memories)
  • increased ventricle size
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7
Q

AD: pathology

A
  • plaques and tangles increases w severity of dementia
  • ß amyloid
  • tau
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8
Q

AD: genetic component- types (4)

A
  • sAPPå (non-amyloidogenic)
  • Aß (amyloidogenic)
  • APP
  • AICD
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9
Q

AD: amyloid hypothesis- 1960s

A
  • plaques + tangles correlate to dementia
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10
Q

AD: amyloid hypothesis- 1985

A
  • plaques composed of 42aa protein (Aß)
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11
Q

AD: amyloid hypothesis- 1987-90s

A
  • precursor gene APP for Aß has mutations linked to some EOAD cases
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12
Q

AD: amyloid hypothesis- 1990s

A
  • mutations in proteins that cleave APP (PSEN1, PSEN2) cause some EOAD cases
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13
Q

AD: amyloid hypothesis- latest discoveries (3)

A
  • Aß toxic to cells in cultures
  • mouse models created that over-express Aß
  • removing Aß in these models prevents cognitive decline
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14
Q

AD: clinical trials- failure rate

A

99.6%

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15
Q

AD: clinical trials- possible reasons they are failing?

A
  • perhaps treatment starting too late?
  • treatment not reaching brain regions affected?
  • disease cascade wrong
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16
Q

AD: alternaive pathological hallmarks (3)

A
  • neuronal cell loss
  • hyperphosphorylated tau
  • neuroinflammation synapse loss
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17
Q

AD: J20 mouse model of alzheimer’s disease- features

A
  • insertion of hAPP w 2 mutations
  • plaque onset by 7 months
  • minimal characterisation
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18
Q

AD: J20 mouse model of alzheimer’s disease- location and results

A
  • hippocampus

- increase in oligomeric Aß and Aß plaques

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19
Q

AD: stereological cell counting technique

A
  • using special square cells that touch the green side/ inside the box are counted
  • those outside or touching red dismissed
20
Q

which comes first: neuronal loss or plaque formation?

A
  • neuronal loss precedes plaque formation
21
Q

AD 1º research: microglia populations increase/decrease in AD progression

A

increase

22
Q

AD 1º research: astrocyte pop during AD progression?

A

will plateau

23
Q

AD 1º research: anxiety and locomotion? J20 mouse model

A
  • in J20 mouse model
  • decreased anxiety
  • increased locomotion
24
Q

AD 1º research: spatial memory and learning in J20 mouse model?

A
  • deficits in both
25
Q

AD 1º research: summary why treating amyloid may be too late in disease

A
  • alternate pathological hallmarks of AD can occur earlier than plaque load in AD mouse model
26
Q

AD 1º research II: can blocking AMPA receptors improve memory + learning? and summary

A
  • yes

- treating neuroinflammation or neuronal cell loss may provide better target for halting disease cascade

27
Q

MND: general features

A
  • lour gehrig
  • amyotrophic lateral sclerosis (ALS)
  • 3-5yr life span from symptom onset
28
Q

MND: upper motor neuron signs (6)

A
  • increased tone
  • hyper reflexia
  • extensor plantar responses
  • spastic gait
  • exaggerated jaw-jerk
  • slowed movements
29
Q

MND: lower motor neuron signs (4)

A
  • mm wasting
  • weakness
  • fasciculations
  • absent/reduced deep tendon reflexes
30
Q

MND: amyotrophic lateral sclerosis (ALS) signs

A
  • combo of both upper and lower motor neuron signs
31
Q

MND: multifaceted approach to diagnosis list (6)

A
  • history
  • neuroimaging
  • physical examination
  • electrodiagnostic studies
  • lab testing
  • genetic testing
32
Q

MND: pathological perspective- list (5)

A
  • spinal cord white matter atrophy
  • loss motor neurons (ant horn SC, motor cortex of brain)
  • ubiquitin-positive inclusions in neurons, frontal cortex, temporal cortex, hippocampus + striatum
  • TDP-43 main component of ubiquitinated inclusions (ALS and FTD patients)
  • neuroinflammation in motor cortex and SC
33
Q

MND: % sporadic and familial

A
  • sporadic 90%

- familial ~10%

34
Q

MND: current treatments (2)

A
  • riluzole

- edaravone

35
Q

MND: mouse model- drugs on grip strength and survival

A
  • no improvement of strength

- no better survival

36
Q

MND: mouse model- neuroinflammation indicators 2wks? before neuron loss

A
  • 16 genes are upregulated
37
Q

MND: mouse model- neuroinflammation indicators 4wks? during neuron loss

A
  • 14 upregulated

- 1 gene downregulated

38
Q

MND: mouse model- CXCL10 protein levels

A
  • 11x increase of protein expression in brain
39
Q

MND: mouse model- CXCL10 protein role in TDP43 rats and location

A
  • upregulation of astrocytes

- spinal cord

40
Q

MND: mouse model- CXCL10 expression how?

A

tissue/cell - protein - 1º antibody - 2º antibody - fluorescein

41
Q

MND: mouse model- TDP43 mouse inflammatory markers

A
  • very similar to humans

- 9/13

42
Q

conclusion: 6 Qs

A
  • humans?
  • mechanism?
  • help/hindrance?
  • best model?
  • therapeutic target?
  • biomarker?
43
Q

current project 1: can reducing CXCL10 rescue mouse phenotype?

A
  • GLUT1 to enhance BBB crossing
44
Q

current project 2: can we model MND in more specific way?

A
  • AAV injection of mutated TDP43
  • visualise in SC
  • grip strength
45
Q

AD vs NMD? similarities and diff (5)

A
  • neurodegeneration (diff areas)
  • neuroinflammation
  • pathology overlap?
  • proteins NOT disease driver?
  • v diff clinical signs

EXP NEURO (10 decks)

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