cognitive impairment and dementia Flashcards
what is dementia
set of symptoms including loss of memory, mood changes, problems communicating etc
what is the most common type of dementia
alzheimers disease (AD)
what term describes dementia gradually getting worse
progressive
what are some examples of origins of dementia
-degenerative e.g alzheimers
-vascular e.g multi infaret dementia
-toxic = alcohol related dementia
-metabolic/endocrine origins
what is AD
progressive, neurodegenerative
early mild symptoms of AD
-lapses of memory/ confusion
-repetition, problem finding words
-decisions are hard
-loss of interest in people and new ideas
-blame others for mislaid items
middle/ moderate symptoms of AD
-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
late/ severe symptoms of AD
-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
what is carried out to diagnose AD
looking into patient history
cognitive tests
physical examination eg blood tests
brain scans
what causes AD
-there is no single cause
-factors include: age, genetics, environment, lifestyle, general health
what kind of studies help disentangle causes of AD
twin studies, particularly MZ twins raised apart (steves et al 2012)
what neural indicators/ markers do researcher tend to focus on now
-neurodegenerative and progressive changes to plaques and tangles (amyloid and tau)
-reduction in neurotransmitters (acetylcholine, glutamate, GABA etc)
what protein forms plaques and tau
plaques = amyloid
tangles = tau
what is the amyloid cascade hypothesis
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
what does Aβ mean
amyloid peptide
NFT =
neurofibrillary tangles
what is a weakness of the amyloid cascade hypothesis
-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
what is the cholinergic hypothesis
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)
how does the cholinergic hypothesis (bowen et al) link to plasticity
-excess of Aβ prevents efficient receptor binding so less neural flexibility present (Lombardo and Maskos 2015)
where do AD treatments often target
ACh receptors
what neurotransmitters does ACh mediate the release of and what do they do
glutamate: plasticity, memory
GABA: attention, inhibiting irrelevant info
what neurotransmitter regulates ACh
dopamine: which is involved in problem solving, motivation, episodic memory etc
age as a risk factor of AD
-greatest risk factor
-factors assosciated with ageing are:
–higher BP
–increased chance of heart disease
–changes to nerve cells and immune system etc
genetics as a risk factors of AD
-APOE e4 allele increases risk of AD
-earlier onset by 14%
model for biological risk factors
alteration in Aβ OR normal Aβ, APOE e4 OR just ageing
lead to…
Aβ aggregation and accumulation
leading to…
toxicity
neuronal cell death
dementia
environmental risk factors of dementia
-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
what is mild cognitive impairment (MCI)
-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
what % of people over 65 have MCI
5-20% (primary amnesic MCI)
what are the 3 types of MCI
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
characteristics of MCI
-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
what is the diagnostic criteria for MCI
-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)
what would a memory clinic include
-lab tests e.g bloods
-MRI scan
-family/ health history
-medical examination
what are the issues diagnosing MCI
-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
MCI and early signs of dementia
-for 15% MCI is prodromal stage of dementia
-risk factors effecting AD can also lead to MCI
-secondary ageing factors may influence MCI
research on the fornix
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
what makes it hard to distinguish MCI patients
alternate pathways due to compensation means performance is quite high so hard to distinguish MCI patients
Metzler and baddeley et al 2013 finding
larger BMI associated with greater loss of integrity in the fornix
why is early identification best
-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
