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Spontaneous spongy degeneration of the brain stem in SAM-P/8 mice, a newly developed memory-deficient strain
H Yagi1, M Irino, T Matsushita
1Department of Neurology, Faculty of Medicine, Kyoto University, Japan.
Abstract:
A spontaneous spongy degeneration of the brain stem and spinal cord was discovered in a murine model of accelerated senescence (SAM), cared for under both conventional (SAM-P/8) and specific pathogen-free (SAM-P/8/Ta) conditions. SAM-P/8 and SAM-P/8/Ta showed no clinical neurological abnormalities, yet there was a deterioration in learning and memory abilities. Light microscopic examination revealed a spongy degeneration in the brain stem and spinal cord, in the reticular formation, and proliferation of hypertrophic astrocytes in the spongy area. The spongiform degeneration progressed with advancing age from four to eight months, after which the entire brain was involved. Astrocytosis increased with advancing degeneration. Ultrastructurally, mild dendritic swelling occurred at one month of age. At two months of age, moderate postsynaptic swelling and a widening of intracellular membrane structure were observed, and at age five months there were large vacuoles circumscribed by membranous lamellae, identifiable as myelin. Vacuoles in SAM-P/8 proved to be swollen neuronal processes and oligodendroglial processes. These SAM-P/8 and SAM-P/8/Ta strains of mice are new memory-deficient strains with spontaneous spongy degeneration associated with aging.
Insights
Accelerated senescence mice develop spontaneous spongy degeneration in the brain and spinal cord, leading to memory deficits. This age-related neurodegeneration involves neuronal and glial process swelling and myelin vacuolation.
Area of Science:
- Neuroscience
- Aging Research
- Pathology
Background:
- Murine models of accelerated senescence (SAM) are crucial for studying age-related changes.
- Spontaneous neurological conditions in aging models can provide insights into disease mechanisms.
Purpose of the Study:
- To investigate spontaneous neurological abnormalities in SAM-P/8 and SAM-P/8/Ta mice.
- To characterize the neuropathology associated with age-related cognitive decline in these models.
Main Methods:
- Light and electron microscopy were used to examine brain stem and spinal cord tissues.
- Histopathological analysis focused on cellular changes, vacuolation, and astrogliosis.
- Behavioral assessments evaluated learning and memory functions.
Main Results:
- Spontaneous spongy degeneration was observed in the brain stem and spinal cord of SAM-P/8 and SAM-P/8/Ta mice.
- Neuropathology progressed with age, involving astrocytosis and vacuolation of neuronal and oligodendroglial processes.
- Despite no overt clinical signs, mice exhibited impaired learning and memory.
Conclusions:
- SAM-P/8 and SAM-P/8/Ta mice develop age-associated spontaneous spongy degeneration.
- These mice represent novel memory-deficient models for studying aging-related neurodegeneration.