Cognitive Aging in Senescence-Accelerated Mouse Models
Summary
Senescence-accelerated mouse models, notably the SAMP8 strain, recapitulate key features of age-related cognitive decline and serve as indispensable tools for investigating mechanisms underlying memory loss and neurodegeneration. These mice exhibit early deficits in spatial and episodic memory, reduced hippocampal neurogenesis, synaptic deterioration and heightened oxidative stress and neuroinflammation. Such changes mirror aspects of sporadic Alzheimer’s disease and other late-life dementias, permitting the interrogation of genetic, epigenetic and environmental factors that drive cognitive ageing. Through behavioural assays, electrophysiology and molecular profiling, researchers can identify critical windows for intervention and test pharmacological and lifestyle strategies. Insights gleaned from SAMP8 and related models have global significance: they inform the design of neuroprotective agents, guide dietary and exercise recommendations for healthy ageing and facilitate the translation of preclinical findings into human clinical trials.
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Cognitive Aging in Senescence-Accelerated Mouse Models publication trend
The graph below shows the total number of articles in cognitive aging in senescence-accelerated mouse models across all publications each year (not limited to Nature Index journals).
Technical terms
Senescence-accelerated mouse models (SAM): Inbred strains, such as SAMP8 and SAMR1, selected for rapid ageing and cognitive decline.
Hippocampal neurogenesis: Generation of new neurons in the dentate gyrus, essential for learning and memory fidelity.
Long-term potentiation (LTP): Prolonged enhancement of synaptic transmission following patterned stimulation, considered a cellular basis for memory storage.
Oxidative stress: Excessive accumulation of reactive oxygen species that overwhelms antioxidant defences, causing molecular and cellular damage.
Neuroinflammation: Glial activation and elevated inflammatory mediators within the brain, frequently linked to age-related cognitive impairment.
References
- Rescue of neurogenesis and age‐associated cognitive decline in SAMP8 mouse: Role of transforming growth factor‐alpha. Aging Cell (2023).
- SVHRSP Alleviates Age-Related Cognitive Deficiency by Reducing Oxidative Stress and Neuroinflammation. Antioxidants (2024).
- Transcriptomics and biochemical evidence of trigonelline ameliorating learning and memory decline in the senescence-accelerated mouse prone 8 (SAMP8) model by suppressing proinflammatory cytokines and elevating neurotransmitter release. GeroScience (2023).
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