CCC- Memory loss in old age, dementia (not finished!) Flashcards
How is dementia more than a memory loss?
It also affects cognitions and behaviour
What is dementia?
Dementia describes a collection of symptoms associated with impaired cognitive abilities and the ability to carry out day to day tasks/ activities.
What are some symptoms of dementia?
Memory loss
Difficulty sustaining attention
Language
Disorientation in space & time
Mood, social & behavioural changes
What are some examples of mood, social & behavioural changes for an individual with dementia?
Can withdraw from social situations.
Become depressed.
Have anxiety/ agitiation/ socially inhibited- gambling.
What is tip of the tongue phenomenon?
The phenomenon of failing to retrieve a word or term from memory.
What is dementia caused by?
Caused by a number of biological diseases- especially chronic & long lasting diseases.
Dementia isn’t a diagnosis in its own right.
Is dementia a normal part of ageing?
NO
What are some causes of dementia?
Chronic diseases- e.g. parkinson’s- neurodegenerative diseases.
Traumatic brain injuries, alcoholism, deficient in certain vitamins
Alzheimer’s disease.
Huntington’s disease.
How prevalent is dementia?
UK- estimated 850,000 people living with dementia.
Roughly 1 in 14 people over the age of 65.
Expected that 2 million people will have dementia by 2050
What is the most common cause of dementia & what is the percentage?
Alzheimer’s disease.
60-70% of cases.
What are other common pathologies which cause dementia?
cerebrovascular disease
Neocortical lewy body disease
If you have multiple pathologies together- are you more/ less likely to experience dementia?
More likely!
What is Alzheimers disease?
Neurodegenerative disease: progressive, irreversible deterioration in cognitive abilities & daily function.
In most people- symptoms of Alzheimer’s disease appear after the age of 60.
What are possible risk factors for dementia?
Stress & anxiety & psychiatric conditions.
How are there individual differences in symptom progression for Alzheimer’s disease?
The way a person experiences the disease- depend on many factors including genes, physical health, personality, emotional resilience, medication they take & support they rely on.
How are there individual differences in symptom progression for Alzheimer’s disease?
The way a person experiences the disease- depend on many factors including genes, physical health, personality, emotional resilience, medication they take & support they rely on.
What is atrophy?
Neuronal loss, reduction in grey & white matter volume.
Topographical disease progression?
Topographical disease progression, starts off in medial temporal lobe, wider temporal regions, parietal & frontal areas, then widespread atrophy (with visual and motor areas spared until late disease stages.
How do you commonly look at atrophy?
Through structural magnetic resonance imaging.
Over the course of Alzhemiers disease- the mass that can be lost can be the size of what?
An orange
Where is a key area that atrophy occurs?
Hippocampus (which has a key role in encoding & memory)
Neurotransmitter production & function is impaired.
How can this be explained?
Synaptic dysfunction- altered communication between neurons.
Loss of cell bodies in Nucleus Basalis of meynert- very early marker of Alzheimers.
These cell bodies are involved in the production of acetylecholine (cholinergic neurotransmitter system)
Medications to reduce dementia symptoms boost brains supply of acetylcholine (which alleviates some of the cognitive symptoms.)
What do medications which reduce dementia symptoms do?
Boost brains supply of acetylcholine (which alleviates some of the cognitive symptoms.)
What abnormalities develop in the proteins required for the maintenance & repair of neurons?
Senile plaques- excess B amyloid protein
Neurofibrillary tangles- misformed tau protein
What do the senile plaques do?
Beta-amyloid protein involved in Alzheimer’s comes in several different molecular forms that collect between neurons.
It is formed from the breakdown of a larger protein, called amyloid precursor protein.
One form, beta-amyloid 42, is thought to be especially toxic.
In the Alzheimer’s brain, abnormal levels of this naturally occurring protein clump together to form plaques that collect between neurons and disrupt cell function
What are neurofibrillary tangles & what do they do?
They are abnormal accumulations of a protein called tau that collect inside neurons.
In Alzheimer’s disease, however, abnormal chemical changes cause tau to detach from microtubules and stick to other tau molecules, forming threads that eventually join to form tangles inside neurons.
These tangles block the neuron’s transport system, which harms the synaptic communication between neurons.
Lead to cell death
How do you measure in vivo
Quantification & localisation of amyloid & tau?
cerebrospinal fluid
bloods
Pet scans (Positron emission tomography)
capturing proteins
How can you quantify the proteins in the spinal fluid?
Doing a lumbar puncture (needle) spinal cord- allows to quantify it.(unpleasant)
Capturing proteins
What do the PET scans do- how do they work?
Inject radioactive tracer into arm
Developed to be specific shape- goes in bloodstream to brain & binds to protein specified
When scan someone- can see where the radioactive substances deposited- shows how much & where the proteins we are trying to target are.
Localisation of amyloid
B-amyloid deposition- where does it first occur?
What are amyloids associated with?
In structures of the default mode network: the posterior cingulate cortex, precuneus, & medial prefrontal cortex.
Cognitive deficits & altered brain activity.
Lifespan approach
What is this ? What does it aim to do?
Reducing the impact of Alzheimers disease.
- Characterizing risk
-Prevention
-Early detection - Monitoring & lifestyle management
Which types of memory are affected by Alzheimers disease?
Episodic memory (short-term, long term)
Semantic memory
Lexicon (vocabulary)
Working memory (flexibility of mental representations)
Spatial memory
How do we assess memory impairment?
Can do quick 10 min pen & paper tests.
Benefits of in clinic memory assessment (quick, easy to administer, widespread adoption)
Novel methods e.g. VR tests of spatial memory, smartphone-based measures.
What is mnemonic discrimination?
Ability to encode & retrieve distinct memories from among events which share common features.
Mnemonic discrimination is a valuable marker of early Alzheimer’s disease.
What are mnemonic discrimination errors?
Are increased in individuals with a diagnosis of mild cognitive impairment.
Correlate with covert alzheimers pathology in older adults without a diagnosis.
Are caused by altered brain functions in memory regions of the medial temporal lobes.
Capturing changes in real word settings- what are the ways we can capture detection’s of alzheimers?
Language- how are they speaking/ are they fluent in their language/ is it declining?
Look at how people walk & their navigation (life space- are they going to new areas or not.)
Sleep-
Everyday life- making tea
What is involved in making a cup of tea?
Multiple cognitive processes.
e.g.
semantic memory- what is tea?
Spatial memory- where is the sugar?
Autobiographic memory- dad likes two sugar?
Working memory- what have I just done?
Making tea-
what are the most common errors made by stroke & closed head injury patients?
Omission- missing out steps in the sequence.
Rusted & Sheppard (2002)
What did their study do?
Longitudinally monitored individuals living with dementia- on their tea making abilities over 5 years.
Different approaches measures tea making abilities.
- Verbal description from memory.
- Observation in own kitchen.
- Observation in novel environment.
- Instructing someone else how to make tea.
Rusted & Sheppard (2002)
What were the results from the study?
People with dementia showed a decrease in the number of steps they could recall- verbally.
When asked to perform- relatively preserved tea making abilities in novel setting & own kitchen.
Shows memories aren’t lost- just difficult to access,
What is the biggest risk factor of Alzheimers disease?
Age
How do our genes play a role in Alzheimers?
Deterministic genes- tied to early onset Alzheimers- account for less than 1% of cases. (chromosome 21, chromosome 14)
Risk genes- associated with higher incidence of Alzheimers - but not sufficient to cause it- linked to sporadic alzheimers disease.
What is APOE e4 associated with?
Substantially greater risk of future Alzheimers disease & poorer cognitive ageing in healthy older adulthood.
Cognitive, structural & functional brain differences from youth.
If have apoe 4 gene - likely to get it at an early age & symptoms will progress quickly,
Changes brains structure & function from childhood & cognitive differences from youth.
What are modifiable risk factors of Alzheimers disease?
Less education
Hypertension
obesity
hearing loss
Smoking
depression
physical inactivity
social isolation
diabetes
How can dementia be prevented/ slowed down?
Lifestyle changes!
e.g. Adherence to meditteranian diet
reduced brain inflammation
stop smoking, obesity
education
cognitive training
rich social network
Summary of Dementia & Alzheimers?
Alzheimers- biological disease- not part of healthy ageing.
(pathologies- amyloid, tau, neurodegeneration)
Memory deficits- key component-not all have it.
Age & genetic factors play a huge role in likelihood of developing dementia- environmental & lifestyle changes can reduce risk- as much as 40%
