The SAMP8 mice develops early abnormalities in learning and memory, These are related to abnormalities in septo-hippocampal function with a decrease in serotonin leading to an increase in GABA and a decrease in acetylcholine. The cognitive defects in these animals are due to overproduction of beta-amyloid and can be reversed by antibodies to beta-amyloid or specific antisense oligonucleotides. The major defect produced by beta-amyloid in these mice appears to be reduction in Delta(9) desaturase activity leading to altered membrane phospholipid content. The SAMP8 mouse appears to be an excellent model to examine the pathophysiology of early defects seen in Alzheimer disease.
机构:
ST LOUIS UNIV, SCH MED, DEPT INTERNAL MED, DIV GERIATR MED, ST LOUIS, MO 63104 USAST LOUIS UNIV, SCH MED, DEPT INTERNAL MED, DIV GERIATR MED, ST LOUIS, MO 63104 USA
FLOOD, JF
MORLEY, JE
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机构:
ST LOUIS UNIV, SCH MED, DEPT INTERNAL MED, DIV GERIATR MED, ST LOUIS, MO 63104 USAST LOUIS UNIV, SCH MED, DEPT INTERNAL MED, DIV GERIATR MED, ST LOUIS, MO 63104 USA
机构:
ST LOUIS UNIV, SCH MED, DEPT INTERNAL MED, DIV GERIATR MED, ST LOUIS, MO 63104 USAST LOUIS UNIV, SCH MED, DEPT INTERNAL MED, DIV GERIATR MED, ST LOUIS, MO 63104 USA
FLOOD, JF
MORLEY, JE
论文数: 0引用数: 0
h-index: 0
机构:
ST LOUIS UNIV, SCH MED, DEPT INTERNAL MED, DIV GERIATR MED, ST LOUIS, MO 63104 USAST LOUIS UNIV, SCH MED, DEPT INTERNAL MED, DIV GERIATR MED, ST LOUIS, MO 63104 USA