Early in the 20th century, Alois Alzheimer first described a disorder of progressive memory loss and confusion in a 50-year-old woman. After she died, he examined her brain and saw that it was full of unusual protein clumps, known as plaques. Over a century later, we know that these plaques are full of a protein called beta-amyloid and are a hallmark of the disease that bears Alzheimer’s name. While other features of Alzheimer’s disease have been discovered, the theory that beta-amyloid is the main cause of this incurable disease has dominated.
A feeling of apathy or being a little forgetful from time to time is nothing unusual. But for some, this could be an early sign of not getting enough thiamine (also known as vitamin B1). Long term, this can have serious consequences, including an increased risk of developing Alzheimer’s disease.
A new study suggests that plaque forming in arteries has much in common with the progression of Alzheimer’s disease. The image shows a cross section of a mouse aorta, the main artery in the body, with a large plaque. Red lines near the top are the wall of the aorta. The plaque contains a dysfunctional buildup of immune cells called macrophages (pink) and protein waste (green)