Cholesterol drugs could help cure Alzheimer’s
The seventh leading cause of death in the United States may finally have a cure, thanks to Washington University medical researchers.
Guojun Bu, professor of cell biology and physiology, and a team of medical students and professors are coming out with some startling results concerning the mystery of what causes Alzheimer’s disease.
More than five million Americans today have Alzheimer’s, a disease that progressively destroys brain cells and causes severe problems with memory, thinking and behavior.
The lab team discovered that a certain class of drug called statins helped to alleviate symptoms in patients with late-onset Alzheimer’s.
Statins are commonly prescribed cholesterol-lowering drugs. But in the Alzheimer’s subjects, Bu and his team noticed how the drugs altered the blood flow to the brain. This alteration in turn affected the regulation of cholesterol in various brain synapses.
“Synapses are very dynamic in their reactions,” said Bu. “That is how we are able to forget things and then remember new things.”
Until recently, one of the main suspects blamed for Alzheimer’s was the build up of amyloid-beta, or A-beta, a peptide that is the main constituent of amyloid plaques in an Alzheimer’s patient’s brain. As these plaques build up over time, blood flow is restricted, leading to eventual problems with the memory.
In early-onset patients, mutations in three different genes produce more sticky peptides than are normal, according to Bu. This leads to the A-beta build-up and clumping, which could lead to Alzheimer’s. Yet early-onset patients only make up about one to five percent of patients.
The majority of Alzheimer’s patients suffer from late-onset Alzheimer’s, a strain of the disease whose cause is essentially unknown.
“It is interesting that early-onset and late-onset Alzheimer’s have different genetic factors, but they lead to the same pathology,” said Bu.
To conduct his research on this “mystery cause” for late-onset Alzheimer’s, Bu and his team used mouse models with specific genes deleted or manipulated. They also used cell models from these mice, often from genetically mutated mice. No patient study was conducted.
Membranes are vital to the formation of synapses and cholesterol makes up the casing around the neurons, affecting the speed at which synapses can be transmitted. Cholesterol also controls proper regulation and activity essential for brain health, which makes its defects detrimental to an Alzheimer’s patient.
Some subjects greatly benefited from the cholesterol-regulating effects of the statins, while others showed no improvement. This difference in reaction among subjects is yet to be determined, resulting in controversy over whether or not the statins are truly beneficial to Alzheimer’s patients.
Still, statins come the closest to affecting the actual disease as opposed to the current drugs available that merely stabilize the symptoms.
“Many clinical studies are currently being conducted with the goal of finding a medicine that might delay the onset of the disease or even cure it altogether,” said Bu.
As for the future of the University’s research, Bu and his colleagues plan to continue to look at Alzheimer’s patients to see whether there is an alteration in cholesterol level or production as the disease progresses. They hope to develop a method to regulate cholesterol transportation and to increase the expression of these transporters.
However, Bu is certainly not alone in his efforts. Over the last several years, there has been an accelerating effort by scientists around the world to treat the disease, delay its onset and hopefully prevent it altogether.
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