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In this enlightening episode, we sit down with Dr. Longo to explore the intriguing role of fasting-mimicking diet (FMD) cycles in reducing Alzheimer's Disease (AD) symptoms and cognitive decline. The FMD cycles have demonstrated considerable potential in decreasing various aging and disease risk factors. As discussed by Dr. Longo, recent studies reveal that these diet cycles can reduce cognitive decline and AD pathology in mouse models more effectively than protein restriction cycles. Furthermore, long-term FMD cycles have demonstrated significant potential in reducing hippocampal Aβ load and hyperphosphorylated tau, enhancing neural stem cell genesis, decreasing the number of microglia, and reducing the expression of neuroinflammatory genes, including NADPH oxidase (Nox2). The deletion of Nox2 in mice or treatment with an NADPH oxidase inhibitor also leads to improved cognition and reduced microglia activation. Preliminary clinical data suggest the feasibility and general safety of FMD cycles in a small group of AD patients. Join us as Dr. Longo takes us through these fascinating findings that indicate FMD cycles' potential to delay cognitive decline in AD models by reducing neuroinflammation and superoxide production in the brain.
Key Words: Fasting-Mimicking Diet (FMD), Alzheimer's Disease, Cognitive Decline, Aging, Disease Risk Factors, Protein Restriction, Neuroinflammation, Superoxide Production, NADPH Oxidase, Neural Stem Cells, Microglia, Aβ Load, Hyperphosphorylated Tau.
Fasting-mimicking diet cycles reduce neuroinflammation to attenuate cognitive decline in Alzheimer’s models https://doi.org/10.1016/j.celrep.2022.111417
By Catarina CunhaIn this enlightening episode, we sit down with Dr. Longo to explore the intriguing role of fasting-mimicking diet (FMD) cycles in reducing Alzheimer's Disease (AD) symptoms and cognitive decline. The FMD cycles have demonstrated considerable potential in decreasing various aging and disease risk factors. As discussed by Dr. Longo, recent studies reveal that these diet cycles can reduce cognitive decline and AD pathology in mouse models more effectively than protein restriction cycles. Furthermore, long-term FMD cycles have demonstrated significant potential in reducing hippocampal Aβ load and hyperphosphorylated tau, enhancing neural stem cell genesis, decreasing the number of microglia, and reducing the expression of neuroinflammatory genes, including NADPH oxidase (Nox2). The deletion of Nox2 in mice or treatment with an NADPH oxidase inhibitor also leads to improved cognition and reduced microglia activation. Preliminary clinical data suggest the feasibility and general safety of FMD cycles in a small group of AD patients. Join us as Dr. Longo takes us through these fascinating findings that indicate FMD cycles' potential to delay cognitive decline in AD models by reducing neuroinflammation and superoxide production in the brain.
Key Words: Fasting-Mimicking Diet (FMD), Alzheimer's Disease, Cognitive Decline, Aging, Disease Risk Factors, Protein Restriction, Neuroinflammation, Superoxide Production, NADPH Oxidase, Neural Stem Cells, Microglia, Aβ Load, Hyperphosphorylated Tau.
Fasting-mimicking diet cycles reduce neuroinflammation to attenuate cognitive decline in Alzheimer’s models https://doi.org/10.1016/j.celrep.2022.111417