Fasting-mimicking diet cycles reduce neuroinflammation to attenuate cognitive decline in Alzheimer’s models

Researchers tested Fasting Mimicking Diet (FMD) cycles in the E4FAD and 3xTg mouse models of Alzheimer's disease, comparing the diet with protein restriction cycles and with controls. In the 3xTg model they ran long-term cycles and measured hippocampal amyloid beta load, hyperphosphorylated tau, genesis of neural stem cells, microglia number and neuroinflammatory gene expression. They also studied mice lacking the Nox2 gene and mice given the NADPH oxidase inhibitor apocynin, and they refer separately to clinical data from a small group of patients with Alzheimer's disease.

The authors reported that the diet cycles reduced cognitive decline and Alzheimer's pathology in both mouse models, with effects they describe as superior to those of protein restriction cycles. In the 3xTg mice they reported reduced hippocampal amyloid beta load and hyperphosphorylated tau, more genesis of neural stem cells, fewer microglia and lower expression of neuroinflammatory genes including Nox2. They reported that mice lacking Nox2, and mice treated with apocynin, also had improved cognition and reduced microglia activation compared with controls. For the human data they say only that the diet cycles were feasible and generally safe in a small group of patients.

The cognitive and pathology findings are from mouse models, not from people, and this is not a study of Prolon. The human element is limited to feasibility and safety in a small group of patients and is not a controlled efficacy result. Nothing here establishes that a fasting-mimicking diet affects Alzheimer's disease or cognitive decline in people.