Diseases & Conditions 

Alzheimer’s Disease : The role of Tangles and Plaques

Alzheimer’s disease is a brain disorder that affects person memory, thinking and behavior. This disease is a form of dementia that is found mainly in people over the age of 65. Alzheimer’s disease accounts for approximately 70 percent of dementia cases.

Alzheimer’s disease was first recorded by Dr. Alois Alzheimer, a German physician who specialized in neuropathology and histopathology, in early 1900’s. One of his patients, a woman names Auguste Deter, had completely lost her memory and developed strange behaviors. When she passed away, Dr. Alzheimer decided to examiner her brain to find out the causes of the symptoms. He noticed two differences that have come to identify Alzheimer’s disease, gumlike clumps outside some cells and an abnormal collection of protein inside other cells. He dubbed these plaques and tangles.

The nutrients from the cell body need to be transported to nerve endings. Inside the healthy brain cells, long threads of proteins serve as tracks for this transport of nutrients.

When scientists examined the brains of patients with Alzheimer disease who had died, they discovered that some of these transport proteins were tangled. Neurons with tangles in their branches could not send nutrient molecules to their nerve endings, and therefore they could not communicate with other neurons. Tangles are found in the cerebral cortex of the brain mainly in the temporal lobe structures.

The second thing Alzheimer took note of was the neuritic plaques. The neuritis plaques are made of a protein called amyloid, normally found in the body. In a person with alzheimer’s disease, large sediments of the protein accumulate between the nerve cells. These plaques were later found to be comprised of deposits of aluminum silicate as well as the amyloid protein.

Amyloid plaques damage the connection points between neurons and interfere with their ability to communicate with one another. Plaques seem to develop initially in the cortical areas in the temporal lobes, which explains why Alzheimer’s patients first develop profound memory loss.

Patients who suffer from a more severe form of Alzheimer disease have far more plaques than those with mild forms. The brains of persons unaffected by Alzheimer can have a few plaques.

Scientists are now on searching to find out why millions of plaques found in the brains of patients with Alzheimer’s disease while very few found in the brains of healthy older peoples.

Amyloid plaques seem to trigger an inflammatory response. In the brain, the inflammatory cells may cause injury simply by their arrival in and around the plaques. The inflammatory process appears to destroy large numbers of brain cell in alzheimer’s patients.

Another contributor to Alzheimer’s disease may be that the natural repair mechanism that rid the body of free radicals is faulty. Apolipoprotein E, which has the potential to protect the lipid membranes against free radical injury, might be less efficient (in repairing the damage) variant in the brain of an Alzheimer’s patients. Without an adequate protection, the free radicals that are brought to the inflammation sites around a plaque can kill nearby innocent neurons too.

Antioxidants such as vitamin E, which aid in the absorption of free radicals, seem to ease the burden of Alzheimer’s disease in some patients.

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