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.
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.
Plaques
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.
