Covers:
- An introduction to Alzheimer's disease
- The pathogenesis and treatment of Alzheimer's disease
- An introduction to Parkinson's disease
- The Pathogenesis and treatment of Parkinson’s disease
An Introduction to Alzheimer’s disease
- Alzheimer’s disease (AD) is a neurodegenerative disease, meaning there is
progressive loss of structure or function of neurons, which can result in the death of
neurons.
- It was first described by Alois Alzheimer in 1906.
- It is a type of dementia, accounting for around 62% of those who suffer from
dementia.
- Prevalence (number of people with the condition at any single point in time) is
around 1 in 127.
- In the U.K. there are around 506,000 people with AD.
- Incidence rates (the number of new cases i.e. of someone becoming ill) ~¼ of the
prevalence rates indicating that disease duration is about 4 yrs.
- Or 8 years duration from onset of symptoms
- There are around 125,000 new cases each year in the U.K.
- It is more prevalent in women than men.
- Only around 44% of those with dementia receive a diagnosis in the UK.
- Two thirds of people with dementia live in the community while one third live in a
care home.
- Hard to diagnose – hard to distinguish between symptom of Alzheimer’s (memory
loss) and age-related memory decline
Diagnosis of AD includes several different things:
• Clinical interview or assessment with patient and informant – help and assist
provision of information (info patients cannot provide)
• Mental and physical health examination
• Blood tests to rule out other conditions
• Structural imaging (CT or MRI) is recommended for all patients
• Amyloid PET imaging if available – a key pathological change
Delays:
- People not sure they have condition – age-related
- Time spent navigating through health services to get to situation they could be
diagnosed
- Person may know but is not willing to face up to problem
- Incorrect diagnosis of lesser forms of dementia
Symptoms:
• Memory loss
• Incorrect language use (forgetting words or using them incorrectly)
• Problems speaking, reading, writing and understanding
• Disorientation in time and space
• Poor or impaired judgement
• Impaired abstract thinking
• Misplacing things
,Psychology and the Brain: Week 8
• Personality changes
• Difficulty with daily functioning
Non-modifiable risk factors AD includes:
• Age is the main risk factor – your risk of developing AD doubles every five years after
the age of 65 years.
• Family history – there is thought to be some genetic component to AD especially the
early onset kind and therefore this is a risk factor.
• Down’s syndrome – individuals with Down’s syndrome are at an increased risk of
developing AD.
- Have 3 copies of chromosome 21 – key proteins found in Alzheimer’s disease is
found in this chromosome
Modifiable risk factors include:
• Several lifestyle factors and conditions associated with cardiovascular disease are
thought to increase the risk of AD.
• Alcohol and cigarette smoking may increase the risk of AD.
• Obesity increases the risk of AD.
• Lower levels of education can also increase risk.
• Social isolation can increase risk of AD.
• Physical exercise/fitness may be a protective factor.
Pathological changes of AD:
• Changes have been found in the brain at both a gross and micro-structure level.
• The most obvious change is a loss of volume particularly to frontal and temporal
areas with enlarged sulci (gaps) between gyri (ridges).
• Loss is pronounced in the hippocampus (critical for memory formation) and rate of
loss of volume is correlated with the rate of loss of cognition.
- General shrinkage of brain – can be seen in CT or MRI scans
, Psychology and the Brain: Week 8
Cellular changes:
• There appears to be selective loss of cholinergic neurons – release acetylcholine
- It is not clear why these neurons are
susceptible to damage.
• The most prominent changes are actually at
a subcellular level and involve two key
proteins:
o Beta Amyloid which is produced
from Amyloid Precursor Protein
(APP) – found between plaque
o Hyperphoshophylated (too much
phosphorus) tau protein which is
formed from normal tau protein.
- These two proteins form amyloid (senile)
plaques and neurofibrilliary tangles throughout the cortex.
Amyloid in healthy brain:
Although the Amyloid Precursor Protein (APP) can turn into beta amyloid which contributes
to AD pathology, APP in itself is not dangerous.
It fulfils a range of useful functions including:
• Synapse formation
• Neuronal plasticity
• Iron regulation
APP is coded for on chromosome 21 (trisomy in
Down’s syndrome).
It is typically cut up by secretase enzymes:
• Alpha-secretase normally cuts it just
outside the cell membrane.
• Gamma-secretase normally cuts it in the
membrane.
• The products are not harmful in anyway.
• In healthy people, this pathway is used 90% of the time
Amyloid in the AD brain:
- In AD it is the actions of a different secretase that is thought to give rise to plaques:
• Beta-secretase normally cuts it higher up than
alpha (further above the cell membrane).
• Gamma-secretase normally cuts it in the
membrane (no change).
• This results in a longer segment, shown in red here
called beta-amyloid. It is believed that this
segment can form the plaques we see in AD.
• The balance between the availability of alpha and
beta secretase therefore determines the likelihood
of the beta/harmful fragment being formed.
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