cognitive impairment and dementia Flashcards

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1
Q

what is dementia

A

set of symptoms including loss of memory, mood changes, problems communicating etc

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2
Q

what is the most common type of dementia

A

alzheimers disease (AD)

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3
Q

what term describes dementia gradually getting worse

A

progressive

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4
Q

what are some examples of origins of dementia

A

-degenerative e.g alzheimers
-vascular e.g multi infaret dementia
-toxic = alcohol related dementia
-metabolic/endocrine origins

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5
Q

what is AD

A

progressive, neurodegenerative

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6
Q

early mild symptoms of AD

A

-lapses of memory/ confusion
-repetition, problem finding words
-decisions are hard
-loss of interest in people and new ideas
-blame others for mislaid items

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7
Q

middle/ moderate symptoms of AD

A

-frequently confused, disorientated, forget names etc
-mood swings
-scared/ frustrated by memory loss
-withdrawal and loss of confidence
-difficulty carrying out everyday activities and need help with daily care

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8
Q

late/ severe symptoms of AD

A

-totally dependent on others for care
-pronounced memory loss e.g cant remember close family
-increasingly frail, more falls etc
-difficulty eating = weight loss
-incontinence
-loss of speech
-aggressive/ distressed

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9
Q

what is carried out to diagnose AD

A

looking into patient history
cognitive tests
physical examination eg blood tests
brain scans

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10
Q

what causes AD

A

-there is no single cause
-factors include: age, genetics, environment, lifestyle, general health

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11
Q

what kind of studies help disentangle causes of AD

A

twin studies, particularly MZ twins raised apart (steves et al 2012)

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12
Q

what neural indicators/ markers do researcher tend to focus on now

A

-neurodegenerative and progressive changes to plaques and tangles (amyloid and tau)
-reduction in neurotransmitters (acetylcholine, glutamate, GABA etc)

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13
Q

what protein forms plaques and tau

A

plaques = amyloid
tangles = tau

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14
Q

what is the amyloid cascade hypothesis

A

Hardy and higgins 1992
-plaques and tangles cause onset of AD
-plaques surround neurons and tangles are inside soma
-abundance of amyloid causes tau tangles that are neurotoxic, causes neuronal cell death and dementia

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15
Q

what does Aβ mean

A

amyloid peptide

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16
Q

NFT =

A

neurofibrillary tangles

17
Q

what is a weakness of the amyloid cascade hypothesis

A

-mere presence of amyloid does not mean AD as healthy adults also have amyloid and tau deposits, its the excess if these that potentially leads to AD

18
Q

what is the cholinergic hypothesis

A

Bowen et al 1976
-evidence for neurotransmission and AD
-acetylcholine (ACh) links to arousal, memory and attention (these all decline in people with AD)
-ACh has widespread projections from basal forebrain influencing activity in rest of brain (including hippocampus)

19
Q

how does the cholinergic hypothesis (bowen et al) link to plasticity

A

-excess of Aβ prevents efficient receptor binding so less neural flexibility present (Lombardo and Maskos 2015)

20
Q

where do AD treatments often target

A

ACh receptors

21
Q

what neurotransmitters does ACh mediate the release of and what do they do

A

glutamate: plasticity, memory
GABA: attention, inhibiting irrelevant info

22
Q

what neurotransmitter regulates ACh

A

dopamine: which is involved in problem solving, motivation, episodic memory etc

23
Q

age as a risk factor of AD

A

-greatest risk factor
-factors assosciated with ageing are:
–higher BP
–increased chance of heart disease
–changes to nerve cells and immune system etc

24
Q

genetics as a risk factors of AD

A

-APOE e4 allele increases risk of AD
-earlier onset by 14%

25
Q

model for biological risk factors

A

alteration in Aβ OR normal Aβ, APOE e4 OR just ageing

lead to…

Aβ aggregation and accumulation

leading to…

toxicity
neuronal cell death
dementia

26
Q

environmental risk factors of dementia

A

-pollution: Chen et al 2017
–pollution is “cause” of 11% of dementia cases

-medical history/health: diabetes, obesity, strokes increase risk
–Lindsay et al 2002: physical exercise has protective function

-social activity: socially active people have slightly reduced chance of dev dementia
– Hsiao et al 2014: interaction reverses mem decline in mice

-mental activity: Baumgart et al 2015
–reading, learning, puzzles mean people less likely to dev dementia

27
Q

what is mild cognitive impairment (MCI)

A

-presence of acquired cog abnormality greater than expected in relation to age and education
-in the absence of dementia
-in the absence of detrimental daily effects upon daily living

28
Q

what % of people over 65 have MCI

A

5-20% (primary amnesic MCI)

29
Q

what are the 3 types of MCI

A

1.amnesic MCI = memory related dysfunction
2.amnesic multi domain MCI = impacts mem and other cog aspects
3.non amnesic MCI = influences many cog aspects but not memory

30
Q

characteristics of MCI

A

-can be transitory (for short time), normal cog function may return to normal
-for some it may be permanent: function does not return to normal, cog declines do not progress much, no dementia development
-only for some MCI represents early stages of AD

31
Q

what is the diagnostic criteria for MCI

A

-subjective decline in STM or LTM (can be determined by someone else)
-objective decline from age and education appropriate mean scores on cog tests
-preserved daily living (Albert 2011)

32
Q

what would a memory clinic include

A

-lab tests e.g bloods
-MRI scan
-family/ health history
-medical examination

33
Q

what are the issues diagnosing MCI

A

-subtle changes to memory, planning, lang, sensory perception etc which is often the case for general ageing so hard to tell the difference
-indiv diff not readily taken into account
-insensitivity of current neuropsychological tests and neuroimaging/ biomarkers (tests not sensitive enough to detect small changes)
-hearing/ visual damage may mean test is not fully understood so pp wrongly diagnosed
-performance dependent on day so could lead to wrong/missed diagnosis

34
Q

MCI and early signs of dementia

A

-for 15% MCI is prodromal stage of dementia
-risk factors effecting AD can also lead to MCI
-secondary ageing factors may influence MCI

35
Q

research on the fornix

A

Metzler and Baddeley 2012
-fornix is 4 white matter tracks with links to episodic memory in brain
-pp with MCI had volume loss in fornix
-shift in memory load/processing resources from fornix to parahippocampul cingulum

36
Q

what makes it hard to distinguish MCI patients

A

alternate pathways due to compensation means performance is quite high so hard to distinguish MCI patients

37
Q

Metzler and baddeley et al 2013 finding

A

larger BMI associated with greater loss of integrity in the fornix

38
Q

why is early identification best

A

-memory complaints may be associated with later dev of MCI/ AD
-jessen et al 2014: concerns regarding memory impairment predict dementia onset 6yrs later
-early identification means support can be put in place