Lecture notes
Causes and treatment of Alzheimer’s Disease
- Module
- MPHARM
- Institution
- University Of Greenwich
This essay type note describes the cause and main treatments for Alzheimer’s Disease.
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Alzheimer’s diseaseAD is a neurodegenerative disease and progressively it destroys nerve cells in the brain. Therefore,
the brain function of memory is lost. AD is a form of dementia disorder. Pathological characteristic
AD is tautopahies. The hallmark of neurodegenerative diseases is that there is misfolding,
aggregation and accumulation of proteins which leads to brain damage. The common protein
aggregate in AD is amyloid beta and hyperphosphorylated tau. AD begins in hippocampus spreads
up to the rest of the brain and there is atrophy in every part of the brain. In AD due to loosing nerve
cells and tissues in region of brain such as hippocampus, the brain function of forming new
memories is lost. They will also find it hard to remember past memories so they will be lost too.
AD cases increase every year. Hallmark of AD was found to be amyloid plaques and tangled bundles
of fibre. The early symptoms of AD are, loosing items, struggling to find the right word in
conversation, forgetting recent events, getting lost in familiar places, forgetting appointments.
Temporal lobe is important for language. AD spreads to rest of the brain. As the disease progresses,
more parts of the brain are lost. Symptoms also increase gradually getting worse. Mini-mental state
exam can be used to test for the severity of the disease. Score above 9 indicates severe dementia
and score of 24 suggests no dementia. MMSE can be used beside brain scans, MRI, PET and physical
examination to diagnose AD.
AD is caused by genetic and environmental factors such as diet. There are two types of AD early
onset and late onset AD.
Early onset AD is typically due to genetics. Occurs in people aged 30-60 years. Caused by mutations
in the genes such as amyloid precursor chromosome 21 (APP 21) , presenilin 1 chromosome 14
(PSEN 1 CH 14) and presellin 2 chromosome 1 (PSEN 2 CH 1). Late onset AD is mostly due to both
genetics and environmental. Occurs in people above 60 years. Most common type of AD. Genetic
factors such as apolipoprotein E.
APP on chromosome 21 is also linked to down syndrome. Studies have also shown people who are
affected by down syndrome has higher risk of AD. Extra copy of APP 21 increases production of
beta-amyloid. It was also found from autopsy studies that high levels of beta-amyloid plaques and
tau tangles were found in down syndrome people by age of 40.
Amyloid precursor protein is coded by APP gene. APP is plasma bound protein. Breakdown of APP
generates harmful forms of amyloid plaques. APP cleavages by secretases alpha beta and gamma. 2
peptides at the beginning must be in ratio of 9:1. A-beta 42 fragment is the most common that is
prone to aggregation.
In non-amyloidogenic pathway APP is cleaved first by a-secretase and then by gamma secretase. In
amyloidogenic pathway APP is cleaved by beta secretase and gamma secretase leads to AB-42
peptide which forms amyloid plaques. Amyloid plaques are toxic.
Apolipoprotein E influences the risk and age of onset of AD. There are 3 alleles of apolipoprotein E
such as epsilon 2,3 and 4. APOE 4 is known to increase the risk for AD and is associated with earlier
age onset. Patients can be tested for APOE 4 allele if AD is suspected. APOE4 leads to atrophy and
neuronal toxicity. Beta amyloid plaques and tau tangles spread throughout brain and disease
progresses.
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