T cells infiltrate the white matter of the aging rhesus monkey brain: Relationship to age-related myelin pathology and cognitive decline
Katelyn V. Trecartin1, Eli Shobin1, Douglas L. Rosene1 1Boston University School of Medicine, Department of Anatomy & Neurobiology
Normal aging, devoid of neurodegenerative disease, is characterized by impairments in executive function, learning and memory. The rhesus monkey is a valuable model to study this process, as the monkey is free of neurodegeneration but still exhibits the same patterns of cognitive decline observed in humans. While cognitive aging was long believed to be due to neuron loss, MRI and stereologic investigations have confirmed that neurons are not lost but instead white matter volume decreases and myelin pathology increases as evidenced by splitting and ballooning of myelin sheaths. Both loss of white matter volume and myelin pathology correlate with age-related cognitive impairment, but the mechanisms underlying this white matter pathology are unknown. In searching for causes, the well documented age-related increases in oxidative stress and inflammation are prime candidates. Several studies from this lab have demonstrated that microglial activation and phagocytosis increase with age and correlate with cognitive decline but it is not clear if this is a response to myelin pathology or a causal factor. In exploring other possible factors damaging myelin we recently found that age-related increases in brain inflammation are accompanied by infiltration of peripheral T cells into white matter where they could become myelin reactive. Here we report the location of infiltrating T cells and quantify their numbers as they relate to age-related myelin pathology and cognitive decline.
(Supported by NIH Grants R01-AG043640andR01-AG042512)
Credits: None available.
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