Age-related defects in lifespan and learning ability in SAMP8 mice.
Pertinent animal models of age-related learning deficiencies are required to elucidate the mechanism of age-related learning deficiencies and to develop novel therapeutic drugs for age-related diseases such as learning defects. Among many strains of accelerated senescence prone, senescence-accelerated mouse (SAM), SAMP8 mice have age-related defects in learning and cognitive abilities. We review recent findings on alterations in SAMP8 brain in neurochemical parameters related to neurotransmission and synaptic plasticity compared to those in SAMR1 brain as the control. In addition, we report the preventive effects of drugs on learning deficiencies in SAMP8 and discuss the usefulness of SAMP8 as an animal model of age-related learning deficiencies.
Nomura
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Y
Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan. nomura@pharm.hokudai.ac.jp
Okuma
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Y
D000375:Aging / Q000502:physiology*; D016564:Amyloid beta-Protein Precursor / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology / Q000502:physiology; D004195:Disease Models, Animal; D018846:Excitatory Amino Acids / Q000378:metabolism; D005911:Gliosis / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism; D007858:Learning / Q000187:drug effects / Q000502:physiology; D008017:Life Expectancy; D008569:Memory Disorders / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D008815:Mice, Inbred Strains; D009473:Neuronal Plasticity / Q000235:genetics; D018697:Nootropic Agents / Q000494:pharmacology; D013569:Synapses / Q000378:metabolism
D016564:Amyloid beta-Protein Precursor; D018846:Excitatory Amino Acids; D018697:Nootropic Agents; D018698:Glutamic Acid