what is AD characterised by
- 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).
How does the risk of AD increase with age?
doubles every 5 years after the age of 65
what are the consequences for society and health provision
people now live longer so more AD patients - £1.2bn
describe mild dementia
memory loss affecting episodic and semantic LTM problems making decisions but can live independently with support
describe moderate dementia
confusion, poor judgement, sundowning (circadian rhythms disturbed)
describe severe dementia
forgetting own identity, unable to communicate and loss of mobility
what are the effects of AD on the brain
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)
describe the importance of beta amyloid plaques in understanding AD
- 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
describe neurofibrillary tangles
- 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
what happens as neurons die in AD
the brain shrinks (atrophy)
- the sulci and the ventricles expand
how are genes involved as a cause of AD
- 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)
how do environmental factors increase the risk of AD
- 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
how early can we detect AD
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
describe MCI
- symptoms of mild cognitive impairment (MCI): remembering appointments and recent events losing train of thought, misplacing everyday items, problems with word finding
when do we class someone as having MCI
milder deficits: may reflect at the earliest stages of dementia but not always, depression, side effects of medication can also produce reversible MCI
how can AD be treated?
- 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
describe vitamin B complex
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
describe treatment options of mild to moderate stages of AD
- 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
describe treatment options of moderate to severe stages of AD
- NMDA inhibitors
- drugs which block glutamate - this is released in large quantities by damaged cells and is toxic to surrounding cells
- mematine
are drugs for AD patients cost effective?
Anti-Alzheimer drugs do not stop the progression of AD, and they only work for some patients. Expensive, with significant side-effects.
how does AD affect episodic memory
- 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
Describe Backman’ study
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
How does AD affect semantic memory
- 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
What causes impairment in object naming
cortical thinning in the left anterior temporal lobe
