Abstract
The pathological findings of the degenerative changes in the brains of SAMP10 mice are reviewed. Following apparently normal brain development, SAMP10 mice developed diffuse atrophy in the cerebral neocortex with advancing age, with the frontal cortex being most severely affected. The entorhinal cortex, amygdala, and nucleus accumbens were also atrophied in aged SAMP10 mice. The number of neurons in the frontal cortex decreased with aging. Terminal deoxynucleotidyl transferase-mediated digoxigenin-labeled dUTP nick end labeling (TUNEL) assays revealed an age-related increase in the number of TUNEL-positive cells, most remarkably in the olfactory tubercle, anterior cingulate cortex, insular cortex and amygdala. These TUNEL-positive cells were interpreted to undergo DNA damage through a mechanism other than apoptosis. Quantitative immunoblots of various brain regions revealed an age-related decrease in the expression of synapse-related proteins, most remarkably in the anterior cerebral neocortex. There were intraneuronal ubiquitinated inclusions in the entorhinal cortex, olfactory bulb (mitral cells), amygdala, piriform cortex, hypothalamus and prefrontal cortex, etc. in aged SAMP10 mice. The pattern of distribution and spread with aging of these inclusions appeared somewhat similar to that of Alzheimer's type neurofibrillary pathology in aging human brains, although the morphology was different.
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