A new study by UF neuroscientists investigated whether accumulations of tau and alpha synuclein, proteins associated with the pathology of Alzheimer’s and other neurodegenerative diseases, can interact to accelerate the appearance of “mixed pathologies” in mouse models.
Mixed pathologies, or multiple protein pathologies occurring simultaneously in the brain, comprise a mix of amyloid beta peptide, tau protein, alpha synuclein protein and even vascular pathologies, but it unknown why and how these mixed pathologies arise. Understanding the extent and distribution of mixed pathologies could help researchers in improving diagnosis, treatment and prognosis.
The study results, published in Brain Communications, were determined using transgenic mouse models – one of tau pathology that recapitulated pathologies found in frontotemporal dementias, Alzheimer’s disease and related syndromes, and another of alpha synuclein pathology that recapitulated features of Alzheimer’s disease and Lewy body dementia.
The investigators found that the combination of tau and alpha synuclein in the mouse model of tau pathology resulted in widespread transmission of pathologies along connected brain regions, but less transmission in a mouse model of alpha synuclein pathology.
In future studies, the research team, led by Paramita Chakrabarty, Ph.D., an assistant professor of neuroscience, and Tosha Williams, a graduate student in Chakrabarty’s lab, hopes to test the potency of mixed pathologies derived from human cases and correlate their distribution with relation to memory impairment to better understand how mixed pathologies are related to increased dementia risk in patients.