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Related Experiment Video

Updated: May 17, 2026

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Published on: March 23, 2011

Vitamin D mitigates age-related cognitive decline through the modulation of pro-inflammatory state and decrease in

Teresita L Briones¹, Hala Darwish

¹Department of Adult Health, Wayne State University, 5557 Cass Ave, Cohn Bldg, Rm 344, Detroit, MI 48202, USA. tbriones@wayne.edu

Journal of Neuroinflammation

|October 27, 2012

Summary

This summary is machine-generated.

Vitamin D supplementation improved cognitive decline in aged rats by reducing inflammation and amyloid-beta burden. These findings suggest vitamin D may be a therapeutic option for age-related memory impairment.

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Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

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Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Published on: December 26, 2016

Area of Science:

Neuroscience
Gerontology
Pharmacology

Background:

Age-related cognitive decline is a growing concern.
Vitamin D is increasingly recognized for its potential neuroprotective effects.
Understanding the mechanisms behind vitamin D's impact on aging brains is crucial.

Purpose of the Study:

To investigate the neuroprotective mechanisms of vitamin D in age-related cognitive changes.
To assess vitamin D's effects on learning, memory, inflammation, and amyloid-beta in aging rats.

Main Methods:

F344 rats (20-month-old and 6-month-old) received vitamin D (1,α25-dihydroxyvitamin D3) or saline for 21 days.
Behavioral tests (water maze, spontaneous object recognition) assessed cognitive function.
Interleukin (IL)-1β, IL-10 levels, and beta-amyloid (Aβ) load/clearance were quantified.

Main Results:

Aged rats showed memory impairment, which was improved by vitamin D.
Vitamin D supplementation normalized increased IL-1β and decreased IL-10 in aged rats.
Vitamin D enhanced Aβ clearance and reduced amyloid burden in aged rats.

Conclusions:

Vitamin D supplementation counteracted age-related increases in inflammation and amyloid burden.
These effects likely mediated the observed memory improvements in aged rats.
Vitamin D presents a potential therapeutic strategy for mitigating cognitive aging effects.