BiotechMashup

Alzheimer's disease has long been studied primarily as a disease of neurons. But researchers have now shown how the disease may be damaging the brain by choking off blood flow. Scientists have revealed that amyloid-², which builds up around brain cells in Alzheimer's patients, interacts with a common blood clotting agent to increase clotting in the arteries that feed the brain. Such activity could cut off blood flow to neurons, suffocating them over time.

(Tufts University, Health Sciences) Researchers have zeroed in on a protein that may play a role in the progression of Alzheimer's disease. The team found that increasing levels of the protein prevented the accumulation of an enzyme linked to Alzheimer's. The strategy may lead to new treatments for the neurodegenerative disease.

Researchers have zeroed in on a protein that may play a role in the progression of Alzheimer's disease. The team found that increasing levels of the protein prevented the accumulation of an enzyme linked to Alzheimer's. The strategy may lead to new treatments for the neurodegenerative disease.

Researchers may be one step closer to slowing the onset and progression of Alzheimer's disease. An animal study shows that by targeting the blood-brain barrier, researchers are able to slow the accumulation of a protein associated with the progression of the illness.

A researcher has discovered that the deadly plaques of Alzheimer's disease interact with certain cellular proteins to inhibit normal signals that maintain blood flow to the brain. Their findings could lead to new approaches to treat the dementia.

Scientists may have uncovered a new explanation for how Alzheimer's disease destroys the brain -- a profusion of blood vessels. They suggest that the growth of capillaries leads to a breakdown of the blood-brain barrier, allowing amyloid beta, the hallmark of the neurodegenerative disease, to be deposited in the brain tissue.

(IOS Press) What are the earliest brain changes associated with the risk of developing Alzheimer's disease? A scientific report published in the October Journal of Alzheimer's Disease finds reduced activity of an energy-generating enzyme in deceased young adult brain donors who carry a common genetic risk factor for Alzheimer's disease -- before the protein changes or microscopic abnormalities commonly associated with the disease and almost five decades before the age at which they might have developed memory and thinking problems.

Increasing a naturally occurring enzyme in the brain slowed the damaging accumulation of tau proteins that are toxic to nerve cells and eventually lead to the neurofibrillary tangles, a major pathological hallmark of Alzheimer's disease and other forms of dementia.

The aggregated proteins strewn about the brain are the hallmark of one of the most common neurodegenerative disorders: Alzheimer's disease. But while these irregular, gunky proteins, called amyloid-beta, are believed to contribute to the deterioration of memory and cognitive ability in Alzheimer's patients, no one knows how they lead to these symptoms. New experiments show how amyloid-beta interacts with a clotting agent in the blood, increasing blood clots that are harder than usual to break down and starving neurons of their regular supply of oxygen.