Cited by 329Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchGenetics, Aging, and Longevity in Model Organisms

Caloric restriction attenuates Aβ-deposition in Alzheimer transgenic models

Patel, Nilay V., Gordon, Marcia N., Connor, Karen E., Good, Robert A., Engelman, Robert W., Mason, Jerimiah, Morgan, David G., Morgan, Todd E. +1 more·2005·Neurobiology of Aging

Abstract

Dietary influences on Alzheimer disease (AD) are gaining recognition. Because many aging processes are attenuated in laboratory mammals by caloric restriction (CR), we examined the effects of short-term CR in two AD-transgenic mice, APP(swe/ind) (J20) and APP(swe) + PS1(M146L) (APP + PS1). CR substantially decreased the accumulation of Abeta-plaques in both lines: by 40% in APP(swe/ind) (CR, 6 weeks), and by 55% in APP + PS1 (CR, 14 weeks). CR also decreased astrocytic activation (GFAP immunoreactivity). These influences of CR on AD-transgenic mice are consistent with epidemiological reports that show that high caloric diets associate with the risk of AD, and suggest that dietary interventions in adult life might slow disease progression.

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Crossref · 10.1016/j.neurobiolaging.2004.09.014

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36 of 36 references verified0 citation errors · 0 not checkable

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  • SIRT1 has protective effects on AD.

    “Patel et al. elucidated the protective effects of SIRT1 on AD, showing that caloric restrictions diminished plaque formation and Aβ levels in the brains of AD transgenic mice models [171].”
  • Caloric restriction diminished plaque formation and Aβ levels in the brains of AD transgenic mice models.

    “Patel et al. elucidated the protective effects of SIRT1 on AD, showing that caloric restrictions diminished plaque formation and Aβ levels in the brains of AD transgenic mice models [171].”
  • Deficiencies in SIRT1 are correlated with enhanced levels of phosphorylated tau in neurons and the number of neurofibrillary tangles in the brains of AD subjects.

    “Consequently, deficiencies in SIRT1 have also been correlated with enhanced levels of phosphorylated tau in the neurons and the number of neurofibrillary tangles in the brains of AD subjects [171,172].”

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Authors
Patel, N. V., Gordon, M. N., Connor, K. E., Good, R. A., Engelman, R. W., Mason, J., Morgan, D. G., Morgan, T. E., & Finch, C. E.
Affiliations
  • University of Southern California (US)
  • University of South Florida (US)
Corresponding author
Morgan, Todd E.
Venue
Neurobiology of Aging
Publisher
Elsevier BV
Published
2005-07
Volume
26
Issue
7
Pages
995-1000
ISSN
0197-4580 (ISSN-L)
OpenAlex
W2089714642
Cited by
329
References
36
Citations by year
2026: 13 · 2025: 6 · 2024: 9 · 2023: 9 · 2022: 13 · 2021: 18 · 2020: 20 · 2019: 19 · 2018: 15 · 2017: 14 · 2016: 16 · 2015: 8 · 2014: 11 · 2013: 20 · 2012: 17
FWCI
10.08
Type
journal article
Language
en
Open access
closed
Locations
  • Neurobiology of Aging (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Keywords
caloric restriction, Alzheimer's disease, amyloid plaques, APP transgenic mice, APPswe, astrocyte activation, glial fibrillary acidic protein, dietary intervention, aging, disease progression
MeSH terms
CD68 Molecule, Alzheimer Disease, Animals, Brain, Disease Models, Animal, Glial Fibrillary Acidic Protein, Humans, Immunohistochemistry, Membrane Proteins, Mice, Transgenic, RNA, Messenger, Antigens, Differentiation, Myelomonocytic, Antigens, CD, Amyloid beta-Peptides, Neurofibrillary Tangles, Reverse Transcriptase Polymerase Chain Reaction, Caloric Restriction, Mice, Presenilin-1, Plaque, Amyloid

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