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Cognitive Deficits, Changes in Synaptic Function, and Brain Pathology in a Mouse Model of Normal Aging(1,2,3)
Martin Weber1, Tiffany Wu2, Jesse E Hanson2
1Department of Neuroscience, Genentech , South San Francisco, California 94080 ; Department of Psychiatry, University of California, San Diego , La Jolla, California 92093.
Eneuro
|October 17, 2015
Summary
Cognitive decline in aging mice is linked to impaired associative learning, not sensory deficits. This study reveals age-related changes in brain function and synaptic plasticity, offering insights into normal aging processes.
Area of Science:
- Neuroscience
- Aging Research
- Cognitive Science
Background:
- Age is the primary risk factor for Alzheimer's disease, but cognitive decline in aged rodents is understudied.
- Sensory and motor impairments in aged animals can complicate cognitive assessments.
Purpose of the Study:
- To investigate age-dependent cognitive, sensory, and motor deficits in mice.
- To examine neural activity, synaptic function, and gliosis during normal aging.
Main Methods:
- Mice aged 3, 11, and 23 months were tested on cognitive, sensory, and motor tasks.
- Postmortem analyses included gliosis and neural activity (c-Fos) markers.
- Hippocampal synaptic function was assessed in brain slices.
Main Results:
- Significant age-related impairments were found in spatial memory and associative learning (active avoidance).
- Sensory functions (vision, hearing) showed some age-related changes but did not fully explain cognitive deficits.
- Increased hippocampal gliosis, decreased neural activity (c-Fos), and impaired synaptic plasticity (reduced synaptic strength, paired-pulse facilitation) were observed in older mice.
Conclusions:
- Age-related cognitive deficits in mice are not solely due to sensory impairments.
- Normal aging involves significant changes in neural function, synaptic plasticity, and gliosis within the hippocampus.
- This study provides a framework for investigating the biology of aging and its impact on cognitive function.
