{"id":10538,"date":"2016-06-30T10:20:19","date_gmt":"2016-06-30T14:20:19","guid":{"rendered":"https:\/\/www.bumc.bu.edu\/biochemcellbio\/?post_type=profile&p=10538"},"modified":"2025-12-22T08:35:59","modified_gmt":"2025-12-22T13:35:59","slug":"david-a-harris","status":"publish","type":"profile","link":"https:\/\/www.bumc.bu.edu\/biochemcellbio\/profiles\/david-a-harris\/","title":{"rendered":"David A. Harris"},"content":{"rendered":"

My laboratory investigates the molecular and cellular mechanisms underlying two classes of human neurodegenerative disorders: prion and Alzheimer\u2019s diseases. Alzheimer\u2019s disease afflicts 5 million people in the U.S., a number that will increase dramatically as the population ages. Prion diseases are much rarer, but are of great public health concern because of the global emergence of bovine spongiform encephalopathy (\u201cmad cow disease\u201d), and its likely transmission to human beings. Moreover, a prion-like propagation mechanism contributes to the spread within the CNS of the protein aggregates that accumulate in other neurodegenerative disorders, including Alzheimer\u2019s disease, Parkinson\u2019s disease, and tauopathies such as frontotemporal dementia.<\/p>\n

Our work has two broad objectives. First, we wish to understand how misfolded protein aggregates, including PrPSc and Alzheimer\u2019s A\u03b2 oligomers, cause neurodegeneration, neuronal death and synaptic dysfunction. Using a variety of model systems, we seek to identify the neuronal and microglial receptors and downstream cellular pathways activated by these protein aggregates. Second, we aim to use our knowledge of the cell biology of prion and Alzheimer\u2019s diseases to develop drug molecules and other therapeutic modalities for treatment of these disorders.<\/p>\n

Postdoctoral Positions are available in the Harris lab<\/a><\/p>\n

Laboratory Members<\/h4>

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