Breakthrough: A new cause of Alzheimer’s found and with it, a possible treatment

Breakthrough: A new cause of Alzheimer’s found and with it, a possible treatment

The research sheds light on the mechanisms that lead to the brain’s failure to prevent the disease. More importantly, it illuminates a path for a cure

Scientists at Trinity College in Ireland believe they have made a groundbreaking discovery about the causes of Alzheimer’s disease and with it, a new path for recovery.

For some time now, it has been known that Alzheimer’s is caused by the buildup of rogue proteins, called amyloid beta, that clump together into plagues and inhibit brain function. In a healthy brain, the bloodstream clears these plagues away. It is the brains unable to clear away the plague that develop Alzheimer’s.

The Irish scientists worked with the Dublin Brain Bank to examine brains that had been affected by Alzheimer’s. They then compared what they saw in laboratory model systems.

The team of researchers has linked the degenerative disease of dementia to the occurrence of deformed blood vessels in the brain. The blood vessels are only slightly out of shape yet that is enough to hinder blood flow from clearing about the plague buildup.

The brain is very strict about what goes in and out via the blood stream. Unlike the rest of the body, there is a delicate tissue, known as the blood-brain barrier (BBB) that acts as a buffer for undesirables. It is believed that a malfunctioning BBB contributes to the buildup. Malformed blood vessels may accelerate the weakening of the BBB.

“We are faced with a condition we don’t fully understand,” said Dr. Matthew Campbell. “We have shown in Alzheimer’s these tight junctions can open and close. And we actually show this molecule amyloid beta can cause the opening and closing itself and allow for its removal.”

The research sheds light on the mechanisms that lead to the brain’s failure to prevent the disease.

“We have shown distinct components of these blood vessels termed tight junctions are altered in Alzheimer’s disease,” said Dr James Kearney, of Trinity College Dublin. “We think this alteration could be a mechanism to allow for the clearance of toxic amyloid beta from the brain in those living with Alzheimer’s disease.”

More importantly, it illuminates a path for a cure.

“The concept of periodic clearance of brain amyloid beta across the BBB could hold tremendous potential for Alzheimer’s patients in the future,” said Campbell. “The next steps are to consider how this might be achieved. Given the recent advances in clinical trials of anti-amyloid beta antibodies, we hope our findings may lead to improved and adjunctive forms of therapy for this devastating condition.”

Alzheimer’s affects 5.3 million Americans. It is the only major cause of death that cannot be prevented, cured, or slowed down.

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