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B&B2 Flashcards

1
Q

what is AD characterised by

A
  • Loss of brain cells with consequent shrinkage of the brain.
  • Psychological symptoms that increase as the disease progresses.
  • Can last 3-20 years, average 7-8 years.
  • Currently no cure (though drugs may boost performance for some people).
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2
Q

How does the risk of AD increase with age?

A

doubles every 5 years after the age of 65

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3
Q

what are the consequences for society and health provision

A

people now live longer so more AD patients - £1.2bn

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4
Q

describe mild dementia

A

memory loss affecting episodic and semantic LTM problems making decisions but can live independently with support

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5
Q

describe moderate dementia

A

confusion, poor judgement, sundowning (circadian rhythms disturbed)

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6
Q

describe severe dementia

A

forgetting own identity, unable to communicate and loss of mobility

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7
Q

what are the effects of AD on the brain

A

in early stages the brain shows reduced levels of glucose (providing energy for cells) and neurotransmitters (chemical that neurons use to communicate with each other)

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8
Q

describe the importance of beta amyloid plaques in understanding AD

A
  • short fragments of beta amyloid protein are released from the membrane of neurons
  • these accumulate as beta amyloid plaques and interfere with the functioning of other neurons
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9
Q

describe neurofibrillary tangles

A
  • healthy neurons contain microtubules which transport nutrients around the cell. A protein called tau plays an important role in the functioning of microtubules
  • in AD, abnormal tau becomes separated from the microtubules causing them to disintegrate
  • twisted strands of tau protein form tangles inside the cell and disabling the internal transport system and causing cell death
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10
Q

what happens as neurons die in AD

A

the brain shrinks (atrophy)
- the sulci and the ventricles expand

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11
Q

how are genes involved as a cause of AD

A
  • mutations occur when a gene is copied incorrectly so if the mutant gene is dominant, its effects will be seen in the organism (phenotype)
  • children have a 50% chance of inheriting the faulty gene and AD
  • the genes responsible for familial AD are found in 3 different chromosomes which all cause a build up of amyloid plaques in the brain (PS1, PS2 and APP)
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12
Q

how do environmental factors increase the risk of AD

A
  • diet (Gu et al) analysed diets of people ages over 65 and after 4 years 12% developed dementia.
  • reduced risk with higher mediterranean diet
  • moderate intake of alcohol may also protect against AD
  • smoking increases the risk in carriers of APOE4
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13
Q

how early can we detect AD

A

to receive an AD diagnosis there must be increasing deficits in at least 2 areas of cognitive functions, severe problems that interfere with everyday activities

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14
Q

describe MCI

A
  • symptoms of mild cognitive impairment (MCI): remembering appointments and recent events losing train of thought, misplacing everyday items, problems with word finding
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15
Q

when do we class someone as having MCI

A

milder deficits: may reflect at the earliest stages of dementia but not always, depression, side effects of medication can also produce reversible MCI

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16
Q

how can AD be treated?

A
  • cognitive stimulation (brain training)
  • exercise and improved nutrition can boost performance in short term and improve mood
  • reminiscence therapy may allow patients to make the best use of early memories
  • no evidence that these change the progression of disease
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17
Q

describe vitamin B complex

A

people with long term alcoholism can suffer from a deficiency of vitamin B1 due to poor absorption to active form
- this causes brain damage and amnesia (damage to hippocampus and related structures)
as well as confabulation and psychosis (damage to frontal lobes)
- these brain regions are implicated in dementia

18
Q

describe treatment options of mild to moderate stages of AD

A
  • cholinesterase inhibitors
  • drugs which boost acetylcholine levels by inhibiting enzymes which break it down
  • about half AD patients show benefits for a limited time
  • donepezil
  • rivastigmine
  • galantamine
19
Q

describe treatment options of moderate to severe stages of AD

A
  • NMDA inhibitors
  • drugs which block glutamate - this is released in large quantities by damaged cells and is toxic to surrounding cells
  • mematine
20
Q

are drugs for AD patients cost effective?

A

Anti-Alzheimer drugs do not stop the progression of AD, and they only work for some patients. Expensive, with significant side-effects.

21
Q

how does AD affect episodic memory

A
  • atrophy in medial temporal lobe
  • earliest signs of AD are often forgetfulness and inability to remember recent events
  • moderate AD - people show disorientation and wandering associated with atrophy in hippocampus
22
Q

Describe Backman’ study

A

Repeated free recall (FR) and recognition (RN) with older adults – the ones with dementia were. Picked and their performance was looked at 3 and 6 years before their diagnosis
The people who went on to develop dementia show lower performance score
Free recall was worse for both groups
Shows that people who develop dementia lose episodic memory first

23
Q

How does AD affect semantic memory

A
  • the left hemisphere is dominant for most aspects of language processing in most people
  • the anterior temporal lobe (lower part) and the inferior frontal lobe (higher part) are important for understanding and producing words. Atrophy here produces semantic and language deficits in AD
24
Q

What causes impairment in object naming

A

cortical thinning in the left anterior temporal lobe

25
Q

how are executive functions impaired in AD

A
  • problems coordinating multiple activities (requires attention to be flexibly allocated to each task)
  • difficulty of each task titrated (by adjusting list length/speed) to match AD patients and controls
  • impaired at dual task condition
26
Q

personality changes in AD

A
  • irritability, agitation, outburst, shouting, fidgeting
  • may be related to lack of cognitive control (following frontal lobe atrophy)
  • apathy: lack of interest in life: failure to initiate actions and thoughts
  • associated with atrophy in or orbifrontal cortex (linked to processing reward value) and frontal pole (linked to high level goals)
27
Q

how does seeing, hearing and moving change as AD progesses

A
  • can see without recognising what they see
  • can hear without understanding what they’re hearing
  • move but without clear purpose
  • primary sensory and motor areas of the brain remain relatively unaffected in AD
  • seeing without understanding can increase hallucinations and talking to tv, misinterpreting shadows etc.
28
Q

describe the case of Iris Murdoch

A
  • studied at oxbridge, wrote 26 novels and 5 books
  • began to develop AD and even though she had a high IQ, it didn’t protect against AD (cognitive reserve hypothesis)
  • impaired on memory tests
  • poor at remembering story details and recognising famous people
  • anomia: word finding problem
29
Q

Top 3 most frequent dementia types

A

62% - AD
17% - vascular dementia
10% - mixed dementia

30
Q

what is vascular dementia characterised by

A
  • loss of cognitive functioning due to disruption of blood supply to the brain (series of small strokes)
  • blocked arteries are most common cause of VD
31
Q

neurological changes/symptoms with VD

A

frontal lobes
- problems with concentration and acute confusion
- problems organising complex thought and behaviour
- behavioural symptoms: apathy and restlessness
- hypertension can cause multiple small strokes that damage the brain over time

32
Q

What is frontotemporal dementia

A

rare but overall but more common in younger people (45-65 yrs old)
- no amyloid plaques
- different forms of FTD depending on where the atrophy is:
- frontal variant in 70% cases (frontal lobes)
- semantic dementia (temporal lobes)

33
Q

frontal degeneration in FTD symptoms

A

personality changes: rude and impatient
- lack of inhibition: inappropriate language and behaviour
- loss of empathy
- compulsive behaviour

34
Q

semantic dementia FTD

A
  • atrophy restricted to anterior temporal lobes bilaterally
  • progressive loss of conceptual knowledge accessed from both words and picture
  • they cannot understand the meaning of words and might recognise objects but not name them
  • other aspects of cognition are spared: these people have their hippocampus preserved so their IQ is largely preserved, good language skills and good memory of recent events
35
Q

symptoms of posterior cortical atrophy

A
  • blurred vision light sensitive
  • progressive inability to recognise faces and objects (agnosia)
  • spatial skills problems like driving
  • impaired reading and writing
  • memory spoken language and thinking preserved until late stages
36
Q

subcortical dementia characteristics

A
  • basal ganglia: subcortical structures involved in starting and stopping movements and thoughts. subcortical dementias that impair the functioning of these structures affect movement and cognitive control
37
Q

describe huntington disease

A
  • excessive movement - inhibitory failure
  • rare (0.01%) genetic disorder causing loss of neurons from mutation of a single gene on chromosome 4 (dominant so 50% change of inheritance)
  • prominent early changes in basal ganglia then cortical atrophy
  • involuntary and excessive movement (hyperkinesia)
  • cognitive changes: aggression anti social behaviour and low mood
  • basal ganglia inhibits thamalus to cortex connection
38
Q

describe parkinsons disease

A
  • loss of dopamine
    affects 1% of 60 yr olds and over 2% of 85 year olds
  • degeneration in substantia nigra causes deficit in neuromodulator dopamine
  • dopamine normally suppresses inhibitory loop (releases movement)
  • symptoms develop slowly and no clinical symptoms until dopamine levels have dropped by 80% (compensation by remaining cells)
39
Q

describe negative symptoms in Parkinson’s

A
  • loss of spontaneous movement (akinesia)
  • slow movement (bradykinesia)
  • disturbed spech
40
Q

define the cognitive reserve

A

high levels of intelligence and education may allow a person to function relatively normal

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