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Basic Science and Pathogenesis.

Amy Christensen1, Cassandra J McGill1, Ali Zaidi1

  • 1University of Southern California, Los Angeles, CA, USA.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 23, 2025
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Summary
This summary is machine-generated.

Longevity treatments like fasting mimicking diet (FMD) and 17α-estradiol (17αE2) reduced Alzheimer's disease (AD) neuropathology in mice. These interventions showed the strongest protective effects in the presence of the APOE4 gene, a key AD risk factor.

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Area of Science:

  • Neuroscience
  • Genetics
  • Aging Research

Background:

  • Aging is the primary risk factor for Alzheimer's disease (AD).
  • The apolipoprotein E4 (APOE4) allele is a significant genetic risk factor for AD and is linked to reduced longevity.
  • Pathways affected by aging and APOE4 are implicated in AD, suggesting longevity interventions may be repurposed for AD treatment.

Purpose of the Study:

  • To investigate the efficacy of two longevity interventions, fasting mimicking diet (FMD) and 17α-estradiol (17αE2), in an Alzheimer's disease mouse model.
  • To determine the independent and combined effects of FMD and 17αE2 on AD neuropathology.
  • To assess the influence of the apolipoprotein E (APOE) genotype (APOE3 vs. APOE4) on treatment efficacy.

Main Methods:

  • Utilized EFAD mice (human APOE3 or APOE4 crossed with 5xFAD AD model).
  • Administered 17α-estradiol (17αE2) and/or a cyclic fasting mimicking diet (FMD) to 16-month-old male mice for nine weeks.
  • Compared outcomes across four groups: vehicle + ad libitum diet, vehicle + FMD, 17αE2 + ad libitum diet, and 17αE2 + FMD.

Main Results:

  • Both 17αE2 and FMD independently reduced Alzheimer's disease neuropathology in a manner dependent on the APOE genotype.
  • The protective effects of FMD and 17αE2 were most pronounced in mice carrying the APOE4 genotype.
  • Combining 17αE2 and FMD did not yield additive therapeutic benefits.

Conclusions:

  • Interventions that enhance longevity show significant potential as therapeutics for Alzheimer's disease.
  • These treatments may be effective even when initiated late in the disease process.
  • Further research and refinement of these translatable interventions are warranted for AD treatment.