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Psychology and the brain > topic 8 (neurodegeneration) lecture 2 & 3(parkinsons) > Flashcards

topic 8 (neurodegeneration) lecture 2 & 3(parkinsons) Flashcards

1
Q

who originally described parkinsons as shaking palsy?

A

James Parkinson

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2
Q

what is parkinsons prevalence?

A

1 in 500

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3
Q

what is disease duration

A

incidence rates is 1/12 of prevalnce this indicates disease duration is approx 12 years

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4
Q

how many new cases of parkinsons is there each year in the uk?

A

500

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5
Q

is it more common in men or women?

A

25% more common in men

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6
Q

what are 3 diagnostic symptoms?

A

shaking that only occurs at rest

slowness of moevement

muscle stiffness

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7
Q

what scans may be used?

A

SPECT scans similar to PET

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8
Q

what are 4 motor symptoms?

A

rigidity and tremor in extremities and head
forward tilt of body
shuffling gait
reduced arm swing

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9
Q

what are 6 non motor symptoms?

A

impaired memory
fluctuating attention
impaired perception
enhanced distractibility
mood problems
dementia

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10
Q

what are risk factors?

A
  1. AGE - affects 1% 60 yrs old but 5% of 85yr olds
  2. GENDER- men more likely. could be less oestrogen or increased head trauma
  3. FAMILY HISTORY
  4. ETHNICITY
  5. HEAD TRAUMA
  6. ENVIRONMENTAL PESTICIDES
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11
Q

what are changes in the brain in PD

A
  • loss of dopaminergic neurons
  • 80% in the substantia nigra compact
  • 50% in the ventral tegmental area

-Lewy bodies- abnormal clumps of alpha synuclein

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12
Q

impact of loss of dopamine

A
  • dopamine neurons in the substantia nigra compact send their axons to the dorsal striatum in the nigrostriatal pathway
  • dopamine enters the striatum and feeds into the limbic associative sensory and motor loops
  • dopamine favours the direct pathway which favours movement so loss of dopamine= loss of movement
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13
Q

is the late onset of parkinsons disease genetic and what type?

A

yes it is considered to be autosomal dominant

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14
Q

what is the genetic type of early onset PD?

A

autosomal recessive

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15
Q

what are 6 processes disrupted or affected in parkinsons disease?

A

protein aggregation- seen by lewy bodies

protein and membrane trafficking

neurite structure

ubuiquitim-proteasome system

mitochondria function

lysosome function

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16
Q

How is oxidative stress related to parkinsons disease?

A
  • oxidative stress is a state of imbalance between the production of reactive oxygen species and their clearance from within the cell.
  • excess reactive oxygen species can cause damage to cell DNA lipids and proteins
  • dopaminergic neurons are 4x more susceptible to ROS damage, possibly due to high calcium loading
  • postmortem PD brains show decrease in antioxidant activity and evidence of ROS mediated damage to lipids and DNA
  • calcium channel blockers which reduce oxidative stress appear to be effective
17
Q

How does inflammation relate to parkinsons disease?

A
  • neuroinflammation is a feature
  • use of antiinflammatory information is associated with a reduced risk of PD
  • not clear whether reaction or cause to the condition
18
Q

what is thought to be the spread of PD?

A
  1. pathology starts in the peripheral nervous system, olfactory system and medulla
  2. it then spreads up through the spinal cord and brain up to multiple cortical regions
    - this has been theorised by looking at the location of lewy bodies that act like a prion disease
    - its thought that dopaminergic neurons could be particuarly prone to death from lewy bodies
19
Q

when considering multifactoral pathogenesis, what are the 3 main proposed causes for loss of dopamine neurons?

A

genetic alterations

oxidative stress

environmental factors leading to mitochondrial dysfunction

20
Q

what are 4 ways of reducing loss of dopamine in parkinsons?

A

increase production

increase release

mimic action

decrease reuptake

decrease breakdown

21
Q

what are 3 treatments for early PD, effectiveness and likelyhood of motor complications

A

LEVODOPA

  • increasews production
  • good effect
  • increases risk of motor complication

DOPAMINE ANTAGONISTS

  • mimic effect
  • moderate effect
  • decrease motor complication risk

MAO-B INHIBITOR

  • prevent breakdown
  • limited effect
  • reduced motor complications
22
Q

how does deep brain stimulation treat parkinsons disease?

A
  • uses an electrode to stimulate parts of the brain
  • helps synchronise basal ganglia pathways
23
Q

how can transplantation treat parkinsons?

A
  • foetal DA cells can be transplanted into the striatum
  • they form connections to host neurons
  • this provides some signs of restoration of function
  • due to these ethical issues stem cells may be used instead
  • issues with stem cells include controlling differentiation and division appropriately

Psychology and the brain (16 decks)

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