Caloric restriction attenuates beta-amyloid neuropathology in a mouse model of Alzheimer's disease.
This study was designed to explore the possibility that caloric restriction (CR) may benefit Alzheimer's disease (AD) by preventing beta-amyloid (Abeta) neuropathology pivotal to the initiation and progression of the disease. We report that a CR dietary regimen prevents Abeta peptides generation and neuritic plaque deposition in the brain of a mouse model of AD neuropathology through mechanisms associated with promotion of anti-amyloidogenic alpha-secretase activity. Study findings support existing epidemiological evidence indicating that caloric intake may influence risk for AD and raises the possibility that CR may be used in preventative measures aimed at delaying the onset of AD amyloid neuropathology.
Wang
Jun
J
Neuroinflammation Research Laboratories, Department of Psychiatry, Mount Sinai School of Medicine, New York, New York 10029, USA.
Ho
Lap
L
Qin
Weiping
W
Rocher
Anne B
AB
Seror
Ilana
I
Humala
Nelson
N
Maniar
Kruti
K
Dolios
Georgia
G
Wang
Rong
R
Hof
Patrick R
PR
Pasinetti
Giulio Maria
GM
D000273:Adipose Tissue; D000544:Alzheimer Disease / Q000378:metabolism / Q000473:pathology* / Q000517:prevention & control; D053829:Amyloid Precursor Protein Secretases; D016229:Amyloid beta-Peptides / Q000032:analysis / Q000378:metabolism*; D000818:Animals; D016282:Aspartic Acid Endopeptidases; D001921:Brain / Q000473:pathology*; D001923:Brain Chemistry; D031204:Caloric Restriction; D050528:Diet, Carbohydrate-Restricted; D004195:Disease Models, Animal; D010450:Endopeptidases / Q000378:metabolism; D005260:Female; D005951:Glucose Tolerance Test; D051379:Mice; D009929:Organ Size; D058225:Plaque, Amyloid / Q000378:metabolism / Q000473:pathology
D016229:Amyloid beta-Peptides; D053829:Amyloid Precursor Protein Secretases; D010450:Endopeptidases; D016282:Aspartic Acid Endopeptidases; C509282:Bace1 protein, mouse