BIN1 is a key regulator of proinflammatory and neurodegeneration-related activation in microglia.
1. Mol Neurodegener. 2022 May 7;17(1):33. doi: 10.1186/s13024-022-00535-x. BIN1 is a key regulator of proinflammatory and neurodegeneration-related activation in microglia. Sudwarts A(1)(2), Ramesha S(3), Gao T(3), Ponnusamy M(1)(2), Wang S(1)(2), Hansen M(1)(2), Kozlova A(4), Bitarafan S(5), Kumar P(3), Beaulieu-Abdelahad D(1)(2), Zhang X(1)(2), Collier L(1)(2), Szekeres C(2), Wood LB(5), Duan J(4)(6), Thinakaran G(7)(8), Rangaraju S(9). Author information: (1)Byrd Alzheimer's Center and Research Institute, University of South Florida, Tampa, FL, 33613, USA. (2)Department of Molecular Medicine, Morsani College of Medicine, University of South Florida, Tampa, FL, 33620, USA. (3)Department of Neurology, Emory University, Atlanta, GA, 30322, USA. (4)Center for Psychiatric Genetics, North Shore University Health System, Evanston, IL, 60201, USA. (5)Parker H. Petit Institute for Bioengineering and Bioscience, Wallace H. Coulter Department of Biomedical Engineering, and Georgia W. Woodruff School of Mechanical Engineering, Georgia Institute of Technology, Atlanta, GA, 30332, USA. (6)Department of Psychiatry and Behavioral Neuroscience, University of Chicago, Chicago, IL, 60637, USA. (7)Byrd Alzheimer's Center and Research Institute, University of South Florida, Tampa, FL, 33613, USA. thinakaran@usf.edu. (8)Department of Molecular Medicine, Morsani College of Medicine, University of South Florida, Tampa, FL, 33620, USA. thinakaran@usf.edu. (9)Department of Neurology, Emory University, Atlanta, GA, 30322, USA. srikant.rangaraju@emory.edu. BACKGROUND: The BIN1 locus contains the second-most significant genetic risk factor for late-onset Alzheimer's disease. BIN1 undergoes alternate splicing to generate tissue- and cell-type-specific BIN1 isoforms, which regulate membrane dynamics in a range of crucial cellular processes. Whilst the expression of BIN1 in the brain has been characterized in neurons and oligodendrocytes in detail, information regarding m
