Neurochemistry, Neuropathology, and Heredity in SAMP8: A Mouse Model of Senescence

• Published in: Neurochemical research 2009-04, Vol.34 (4), p.660-669
• Main Authors: Tomobe, Koji, Nomura, Yasuyuki
• Format: Article
• Language: English
• Subjects: Aging - genetics; Aging - metabolism; Aging - pathology; Amyloid beta-Peptides - metabolism; Animals; Biochemistry; Biomedical and Life Sciences; Biomedicine; Brain - metabolism; Brain - pathology; Cell Biology; Cognition Disorders - genetics; Cognition Disorders - metabolism; Cognition Disorders - pathology; Dendritic Spines - pathology; Heredity; Mice; Mice, Inbred Strains; Mitochondria - physiology; Models, Animal; Nerve Net - pathology; Nerve Net - physiology; Neurochemistry; Neurodegenerative Diseases - genetics; Neurodegenerative Diseases - metabolism; Neurodegenerative Diseases - pathology; Neurology; Neurosciences; Oxidative Stress; Phosphorylation; Review Article; tau Proteins - metabolism
• ISSN: 0364-3190; 1573-6903
• DOI: 10.1007/s11064-009-9923-x

The SAMP8 strain spontaneously develops learning and memory deficits with characteristics of aging, and is a good model for studying the mechanism of cognitive dysfunction with age. Oxidative stress occurs systemically in SAMP8 from early on in life and increases with aging. Neuropathological changes such as the deposition of Aβ, hyperphosphorylation of tau, impaired development of dendritic spines, and sponge formation, and neurochemical changes were found in the SAMP8 brain. These changes may be partially mediated by oxidative stress. Oxidative damage is a major factor in neurodegenerative disorders and aging. A decline in the respiratory control ratio suggesting mitochondrial dysfunction was found in the brain of SAMP8. The rise in oxidative stress following mitochondrial dysfunction may trigger neuropathological and neurochemical changes, disrupting the development of neural networks in the brain in SAMP8.