Protein restriction cycles reduce IGF-1 and phosphorylated Tau, and improve behavioral performance in an Alzheimer's disease mouse model

A study of periodic protein restriction cycles in a mouse model of Alzheimer's disease. The intervention is not the Fasting Mimicking Diet.

Aging Cell, 2013. Parrella E, et al.

Funding and competing interests (from the paper, shortened): This study was supported, in part, by a NIH Grant P01 AG034906 to VL.

Connection to Prolon: Valter Longo, one of the authors, is the founder of L-Nutra, Prolon's parent company.

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Study type
Animal study (mice) (not about the FMD)
Journal
Aging Cell
Published
2013
Authors
Parrella E, et al.
DOI
10.1111/acel.12049
PubMed ID
23362919

Summary

This is an animal study of protein restriction, not of the Fasting Mimicking Diet and not of Prolon. Researchers gave four months of periodic protein restriction cycles, with supplementation of non-essential amino acids and without calorie restriction, to mice that already had significant cognitive impairment and Alzheimer's-like pathology. Circulating IGF-1 and IGFBP-1, amyloid beta levels, hippocampal tau phosphorylation and cognitive performance were measured.

The authors reported that the protein restriction cycles reduced circulating IGF-1 by 30% to 70% and caused an eight-fold increase in IGFBP-1. They reported that the cycles did not affect amyloid beta levels. They reported decreased tau phosphorylation in the hippocampus and reduced age-dependent impairment in cognitive performance. They describe the results as indicating that protein restriction cycles without calorie restriction can promote changes associated with protection against age-related neuropathologies.

This paper has no Fasting Mimicking Diet content and does not evaluate Prolon. The intervention is periodic protein restriction with amino acid supplementation, which is a different dietary approach, and it was given to mice rather than to people. One of the measured outcomes, amyloid beta, did not change. The paper belongs here as background literature about protein restriction and growth factors, not as evidence about any product.

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