Alzheimer’s Disease (AD), Pathology and Genetics, Animation.


Alzheimer’s disease, or AD, is a very common
neurodegenerative disorder in which brain cells are progressively damaged and die, leading
to loss of memory, thinking skills and eventually all other brain functions.
A brain consists of billions of neurons, or nerve cells, which communicate via chemical
messages, or neurotransmitters. This communication occurs in a space between neurons, called
a synapse. Neuron communication is essential to all brain activities.
An Alzheimer’s brain is characterized by presence of abnormal plaques and tangles.
Plaques are clumps of a peptide known as beta-amyloid. Beta-amyloid derives from a larger membrane
protein normally present on the surface of nerve cells. These clumps are toxic to nerve
cells and may block cell-to-cell signaling at synapses. They are also believed to trigger
inflammation responses that bring further damage to the brain tissue.
Tangles are formations of a protein named tau. Tau protein’s major function is to
stabilize axonal microtubules – the tubular structures that run along axons of neurons
and are responsible for intracellular transport. In AD patients, tau molecules are mis-folded
and clump into tangles. As a result, the microtubules are disintegrated and cellular transport is
impaired. As the toxic deposits of plaques and tangles
increase, neurons stop functioning, lose connections with each other, and die.
The damage initially takes place in the hippocampus, the part of the brain that is essential in
forming memories. That is why short-term memory loss is usually one of the first symptoms
of Alzheimer’s. Plaques and tangles tend to spread through the cortex in a predictable
pattern as the disease progresses. New symptoms appear accordingly and in an order that corresponds
to different stages of the disease. At the final stage, the brain shrinks dramatically
and nearly all its functions are affected. Most people with Alzheimer’s show first
symptoms after the age of 65, while the process of neuron destruction has probably started
many years earlier. For this form of late-onset AD, the cause remains largely unknown, but
a combination of environmental and genetic factors is likely. Notably, a certain form
of a lipoprotein named Apolipoprotein E is shown to increase susceptibility to the disease.
For a small subset of AD cases known as Familial Alzheimer’s Disease, genetic factors have
been identified. This rare form of AD is linked to a mutation in one of several genes involved
in beta-amyloid production. For this group, the disease strikes earlier in life, commonly
between 50 and 65 years of age, but can be earlier.
Currently there is no cure for Alzheimer’s. Treatments aim to slow down the process of
destruction and relieve symptoms to improve quality of life for patients and caregivers.

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