Is the simplistic concept that too much amyloid causes late-life Alzheimer’s correct? No. Absolutely not. In the 1960s some researchers proposed the hypothesis that too much accumulation of a protein called Amyloid can cause shrinkage in the brain which then leads to dementia (called Amyloid Cascade Hypothesis). Initially, it looked like we were finally going to cure Alzheimer’s disease once and for all. But more and more research failed to show that amyloid plaques “cause” brain shrinkage.
Pharmaceutical companies spent billions of dollars on finding drugs that reduce levels of amyloid in the brain. They were successful in doing this, but the patients who took the drug did not improve. Many pharmaceutical companies finally realized that amyloid may not be the key target for prevention or treatment of Alzheimer’s disease, but the research community in this field keeps pushing the cascade hypothesis.
I think Amyloid is likely a marker for damage to the brain, more so than being the culprit itself; it is the smoke, not the fire. Lack of sleep, concussion, and vascular risk factors have all been associated with too much amyloid in the brain. We need to focus on factors that have been shown to improve brain health, such as exercise, diet, and quality sleep for ways we can prevent late-life cognitive decline.