Tau pathology in neurons and glial cells of aged baboons.

Abstract

The formation of cytoskeletal alterations associated with abnormally phosphorylated microtubule-associated tau protein is emerging as a common pathomechanism in several neurodegenerative diseases of the human brain. These disorders include Alzheimer’s disease (AD), the most common and most extensively studied disorder associated with abnormal tau protein’. Tau pathology is also seen in other “tauopathies” including corticobasal degeneration, Pick’s disease, progressive supranuclear palsy, and argyrophilic grain disease2,3,4. These diseases are characterized by taupositive inclusions deposited not only in nerve cells but also in glial cells3,5Finally, tau pathology develops in some families afflicted with hereditary frontotemporal dementia and parkinsonism linked to chromosome 176,7. Interestingly, FTDP-17 recently has been linked to a number of pathogenetic mutations of the tau gene8. At this point, the mechanisms of tau pathology in neurons and glial cells are not fully understood Animal models replicating characteristics of human tauopathies could provide information not obtainable from studies of the human brain. In an earlier report, we demonstrated the existence of neuronal and glial tau pathology in two out of four aged baboons9. Subsequently, we extended our sample to a total of 50