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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.
