Sciatic Nerve Injury Pathology

Alzheimers Disease AD Pathology and Genetics Animation

Alzheimer's disease, or AD, is a very commonneurodegenerative disorder in which brain cells are progressively damaged and die, leadingto loss of memory, thinking skills and eventually all other brain functions.A brain consists of billions of neurons, or nerve cells, which communicate via chemicalmessages, or neurotransmitters. This communication occurs in a space between neurons, calleda 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 betaamyloid. Betaamyloid derives from a larger membraneprotein normally present on the surface of

nerve cells. These clumps are toxic to nervecells and may block celltocell signaling at synapses. They are also believed to triggerinflammation responses that bring further damage to the brain tissue.Tangles are formations of a protein named tau. Tau protein's major function is tostabilize axonal microtubules – the tubular structures that run along axons of neuronsand are responsible for intracellular transport. In AD patients, tau molecules are misfoldedand clump into tangles. As a result, the microtubules are disintegrated and cellular transport isimpaired. As the toxic deposits of plaques and tanglesincrease, 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 informing memories. That is why shortterm memory loss is usually one of the first symptomsof Alzheimer's. Plaques and tangles tend to spread through the cortex in a predictablepattern as the disease progresses. New symptoms appear accordingly and in an order that correspondsto different stages of the disease. At the final stage, the brain shrinks dramaticallyand nearly all its functions are affected. Most people with Alzheimer's show firstsymptoms after the age of 65, while the process of neuron destruction has probably startedmany years earlier. For this form of lateonset

AD, the cause remains largely unknown, buta combination of environmental and genetic factors is likely. Notably, a certain formof 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 havebeen identified. This rare form of AD is linked to a mutation in one of several genes involvedin betaamyloid production. For this group, the disease strikes earlier in life, commonlybetween 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 ofdestruction and relieve symptoms to improve

quality of life for patients and caregivers.

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