Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuroscience and behaviour > Alzheimer's > Flashcards

Alzheimer's Flashcards

1
Q

neurodegeneration

A

progressive damage or death of neurons leading to a gradual deterioration of the bodily functions controlled by the affected part of the nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

neurodegenerative disorders

A
  • Acute e.g. stroke
  • Chronic e.g. Alzheimer’s, Parkinson’s, Huntington’s
  • Natural degeneration i.e. ageing
  • Disease-induced degeneration e.g. Alzheimer’s disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

dementias

A
  • Dementia - umbrella term for a particular group of symptoms, not a specific disease
  • Characteristic symptoms of dementia = mem, lang, problem-solving, other cog abilities
  • Dementia has many causes
  • Alzheimer’s disease = most common cause of dementia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

alzheimer’s disease

A
  • First identified over 100yrs ago
  • ‘A degenerative brain disorder of unknown origin that causes progressive memory loss, motor deficits, and eventual death’
  • Incidence increases as population ages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

alzheimer’s prevalence

A
  • 50m worldwide
  • 1m UK
  • 1 in 14 ppl aged over 65
  • At current rate - over 1.5m ppl in UK by 2040
  • Access to diagnosis/treatment/support
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

alzheimer’s risk factors

A
  • non-modifiable risk factors
  • modifiable risk factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

non-modifiable risk factors

AD

A
  • age
  • bio sex
  • genetics
  • family history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

age

non-modifiable risk factors AD

A
  • Most important - as age increase the chances
  • Ageing != Alzheimer’s disease
  • 65-74yrs: 3%
  • 75-84yrs:17%
  • Over 85: 32%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

bio sex

non-modifiable risk factor AD

A
  • x2 as many women over 65 with AD vs men
  • Lifespan expectancy males vs females - female life expectancy is 3.6yrs greater than for males in 2016 - increasing the chances
  • 65-69yrs: AD prevalence 0.7% females: 0.6% males
  • 85-89yrs: AD prevalence 14.2% females: 0.8% males
  • Sex diffs in longevity, hormonal events over lifespan, underlying disease, disease progression, response to treatments
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

modifiable risk factors

AD

A
  • cardiovascular disease risk factors
  • relationship between cardiovascular system & brain function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

relationship between cardiovascular system & brain function

modifiable risk factors AD

A
  • Brain - consumes 20% of the blood’s oxygen & energy supplies
  • Brain function - reliant on healthy heart & blood vessels
  • Impaired blood flow = increases risk of dementia/AD
  • Fatty plaques
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

impact of alzheimers

A
  • Patients, family members, carers
  • NHS, social services, society
  • Total cost of dementia care (UK) = £26.3b per annum (NHS, private social care, local authority care): not just AD
  • Desire for care but also to try to eliminate from inds & society
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

symptoms

AD

A
  • continuum
  • brain changes - progress - noticeable symptoms
  • preclinical –> MCl –> mild –> moderate –> severe
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

early stages

AD

A
  • Changes in brain function aren’t sufficient to = symptoms
  • Compensatory mechanisms activated?
  • Some changes in brain function may occur up to 20yrs before symptoms e.g. beta-amyloid levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

early signs

AD

A
  • Normal ageing? - might disregard symptoms due to it possibly being due to getting older
  • ‘blunting of emotional responses’
  • Social withdrawal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

memory impairment

AD

A

Progressive memory loss (initially episodic & declarative)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

impairment in function

AD

A
  • Mem
  • insight
  • judgement
  • lang
18
Q

changes in personality

AD

A
  • apathy
  • indifference
  • depression
19
Q

presentation of symptoms dependent on

AD

A
  • Stages of disease
  • Age of ind
  • Sex of ind
  • Other underlying conditions/medication
  • Patient vs carer reporting
  • Access (real or perceived) to diagnosis
20
Q

later stages

AD

A
  • time course varies widely
  • Onset of symptoms - death ~ 10yrs
21
Q

advanced stages

AD

A
  • Gross disorientation in time & place
  • Total dependence on carer for ‘everyday’ tasks
  • Inability to comprehend/communicate
  • Little awareness of past or future
  • Little movement - difficulty in swallowing - infections e.g. sepsis, pneumonia
22
Q

AD causes

A
  • not a single cause of AD
  • Most likely develops from multiple factors - genetics, lifestyle & environment
  • Majority of cases (99%) not hereditary
  • Not related to whether you have a family member with AD
23
Q

what causes brain dysfunction associated with AD

A
  • accumulation of the protein fragment beta‐amyloid (called beta‐amyloid plaques ) outside neurons
  • accumulation of an abnormal form of the protein tau (called tau tangles ) inside neurons
  • most prominent brain changes associated with Alzheimer’s
24
Q

types of AD

A
  • early-onset
  • later-onset
25
Q

early onset AD

A
  • caused by gene mutations on chromosomes
  • Autosomal dominant inheritance
  • If 1 of these mutated genes is inherited from a parent - person will almost always develop early onset AD
26
Q

late onset AD

A
  • genetic risk factors involved
  • apolipoprotein E
  • apoE & beta-amyloid
  • most cases are sporadic
27
Q

apolipoprotein E

late onset AD

A
  • Gylcoprotein, transports cholesterol in blood, plays a role in cellular repair
  • On chromosomes 19, the apoE gene has 3 common forms or alleles: E2, E3, E4
  • Presence of E4 increases risk of developing AD - not cause
28
Q

apoE and beta-amyloid

late onset AD

A
  • Normally – beta-amyloid is soluble
  • BUT…becomes insoluble when ApoE4 attaches to it
  • Therefore, more likely to be deposited in plaques
  • Presence of ApoE4
  • Increases deposits of b-amyloid and formation of plaques
29
Q

pathology

AD

A
  • brain atrophy
  • cellular level features: senile plaques, neurofibrillary tangles
  • synaptic loss
  • selective depletion of neurotransmitter systems
30
Q

brain atrophy

AD pathology

A
  • brain shrinking in AD patient more so than normal
  • Less surface areas
  • Less volume
  • AD = sever degeneration of the hippocampus, cerebral cortex & ventricular enlargement
31
Q

senile plaques

cellular level features

A
  • more in AD
  • Location is diff - hippocampus
  • increased portion of long form
  • long form - less soluble, more likely to accumulate
  • induce synaptic dysfunction, disrupt neuronal connectivity & result in neuronal death
  • weak correlation in quantity and distribution + AD
32
Q

neurofibrillary tangles (tau tangles)

cellular level features AD

A
  • Non-AD brains – tau binds to and stabilizes microtubules (nutrient transport system)
  • AD – tau detaches and sticks to other tau molecules, disrupts cell’s transport system
33
Q

synaptic loss

AD

A
  • Extensive
  • Depletion of selective neurotransmitter systems
  • Acetylcholine (Ach)
  • Glutamate
  • Serotonin
  • Noradrenaline
34
Q

selective loss of neurotransmitter systems

AD

A
  • Neurones that use Ach or glutamate are particularly affected
  • Also, neurones that utilise serotonin or noradrenaline are affected
35
Q

cholinergic hypothesis of AD

A
  • Degeneration of Ach producing neurones in forebrain
  • Deficit in Ach producing enzyme
36
Q

treatment options

AD

A
  • psychological
  • pharmacological
  • caregiving
37
Q

psychological approaches

treatment AD

A
  • memory aids
  • CBT
  • music therapy
  • structured social interaction
  • stimulated presence therapy
38
Q

caregiving

AD treatment

A
  • Attending to another person’s health needs and well-being
  • Assisting with activities of daily living
  • Emotional and practical support
  • Managing medications/health service interactions
39
Q

pharmacological approaches

AD treatment

A
  • cholinergic drugs - boosts activity at cholinergic synapses
  • glutamate receptor antagonists - protects brain cells from toxic effects of excessive levels of glutamate
40
Q

treatment approaches in development

AD

A
  • Strategies to reduce b-amyloid accumulation: anti-inflammatory agents, enzyme inhibitors (decrease production of b-amyloid)
  • Strategies to reduce tau aggregation, anti-inflammatory agents
  • Improving cardiovascular health
41
Q

biomarkers

AD

A
  • CSF levels/changes of B-amyloid and/or tau
  • Blood tests of brain-derived products
  • Brain imaging studies:
  • MRI/CT – structural changes in brain (need age comparison)
  • Amyloid or Tau PET scans – to examine accumulation of amyloid/tau
  • Fluorodeoxyglucose PET scans – to examine energy i.e. glucose, use in brain

Neuroscience and behaviour (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions