Researchers and pharma companies have tried to attack this disease by reducing amyloid plaques, but inflammation may be the real culprit.
Alzheimer’s is still a disease that is routinely diagnosed only after death and autopsy. Then, it is easy to recognize the disease’s cardinal features: a shrunken brain dotted with amyloid plaques interspersed among neurons containing tangled fibrils, which may also contain inclusions similar to those found in the brains of Parkinson’s patients. These irrefutable histological markers of Alzheimer’s have led the majority of researchers to conclude that amyloid plaques are the pathogenic entity of the disease. But there is still no smoking gun that definitively singles out the plaques as the causative agent. Amyloid is the scientific equivalent of a culprit assumed guilty until proven innocent. Although many pharmaceutical companies vigorously took aim at amyloid, so far there is no unequivocal evidence that clearing plaques in Alzheimer’s disease results in cognitive improvement, suggesting that amyloid plaques may be end-stage rune stones of neuronal damage initiated by genetic variations, brain trauma, and aging.