. It was long believed that amyloid beta-protein plaque in the brain triggered neurodegeneration by strangling brain nerve cells: The plaque was thought to cause tangles made of another protein, called tau, within the nerves.
Battling amyloid became the nexus of research, and thus funding, into pharmaceuticals and cures for Alzheimer’s — to the detriment of other research avenues, Perlmutter says. But this explanation of Alzheimer’s pathology came under suspicion following 2022 reports of fraudulent past ¬research, as well as other findings.
Now, many experts are shifting the focus away from amyloid plaques and toward metabolism. “What makes a good brain go bad ultimately turns out to be a metabolic change,” Perlmutter explains. “It is a bioenergetic issue: a failure of the brain’s ability to supply blood to itself and to use the fuel in that blood, which is glucose, to power itself.”
A 2017 review published in Frontiers in Aging Neuroscience details the metabolic failure and connection between Alzheimer’s Disease and insulin resistance. It highlights research that finds brain-glucose hypometabolism, or decreased brain-glucose consumption, may occur decades before clinical manifestations of Alzheimer’s.
In addition, the authors report that people with insulin resistance or type 2 diabetes have an increased risk of developing the disease.
“Now, using PET [positron emission tomography] scans and even more recently MRI [magnetic resonance imaging], we can detect and predict who’s going to have Alzheimer’s based on the loss of energy utilization — even when there’s no clinical issue like memory failure,” says Perlmutter.
With a better understanding of Alzheimer’s pathology, scientists could better focus on a preventive prescription.