|
| |
Alzheimer’s, an age related disease, slowly
destroys cognitive functioning such as loss of memory and thinking skills. The
disease causes shrinkage of the brain. The build up of plaques (beta amyloid
protein in the spaces between neurons) and tangles (twisted protein tau that
builds up inside cells) in the brain are believed to be the main causes of brain
shrinkage. How plaques and tangles reduce brain volume is still unclear.
Scientists say that plaques and tangles block communication among neurons,
resulting in their death. It is believed that death of neurons causes
Alzheimer’s disease. Healthy brains form plaques, but they don’t allow them to
get accumulated in between the neurons. The diseased brains, however, can’t
prevent such accumulation.
Alzheimer’s is also related to heart condition. This means any heart disease,
diabetes, stroke, high blood pressure and high cholesterol can potentially
increase the possibility of Alzheimer’s disease. New study, as reported in
Technology Review, says that a genetic variation linked to longevity may protect
against the development of Alzheimer’s disease and dementia. This variant
affects cholesterol metabolism boosting high levels of high-density lipoprotein
(HDL). In a way it suggests that good cholesterol enhancing drugs can help in
the prevention of Alzheimer’s disease.
The scientists of Albert Einstein College of Medicine in New York made an
interesting observation: A specific variation of the longevity gene responsible
to produce cholesterylester transfer protein (CETP) is more commonly found in
very long-lived people. They found that those with two copies of the protective
variant had a 70 per cent lower chance of developing Alzheimer's and other
dementias. It also showed the potential of significantly lowering the rate of
memory decline.
Researchers are not sure what role the genetic variation plays in the brain.
They speculate that “it helps get blood into the brain … and anything that
preserves blood flow to the brain is helpful." A handful of CETP inhibitors to
raise good cholesterol without increasing blood pressure are now in clinical
trials. Their acceptability will only be established when their role in
preventing heart disease is more clearly understood. It will largely depend upon
if such inhibitors can meet the long-term safety requirements.
We know that healthy life style can prevent one from the drudgery of many
devastating diseases, including Alzheimer’s. It is believed that frailty and
Alzheimer’s disease possibly share a common cause. It means that chronologically
old but biologically young people can have nearly normal long life. This indeed
is the observation of scientists at the Salk Institute of Biological Studies.
Researchers of this institute modulated the aging process of mice by modulating
insulin like growth factor 1 (IGF-1) signalling pathway, known for regulating
lifespan and youthfulness. The IGF-1 is one of the most potent natural
activators of cell growth and proliferation, and a potent inhibitor of
programmed cell death.
It has been reported that nutritious diet, physical fitness, social engagement,
and mentally stimulating activities are potential factors, which help in
reducing the risk of cognitive decline and Alzheimer’s disease. Scientists are
therefore looking at many possible interventions, such as cardiovascular and
diabetes treatments, antioxidants, immunisation therapy, cognitive training, and
physical activity to slow down, delay or prevent Alzheimer’s disease.
The writer is a biotechnologist and ED, Birla Institute of
Scientific Research, Jaipur
- http://www.mydigitalfc.com
| |
|
