Biography

Dr. Wisniewski is a Professor of Neurology, Pathology and Psychiatry at NYU. He serves as the Director of the Center for Cognitive Neurology, and the Director of the Conformational Disorders Laboratory, as well as being the Co-Director of the NIH funded Alzheimer’s Disease Center. In addition, he is the Director of the NYU Neuropathology Core, and the Director of the Neuropathology Fellowship. He obtained his medical degree at King’s College, London in 1983 and is board certified in Neurology and Neuropathology. He did his Neurology residency at NYU and his Neuropathology training at Columbia-Presbyterian Medical Center. He was a Chief Resident of Neurology and of Pathology at NYU and Columbia-Presbyterian, respectively. After completing his Neuropathology training he returned to NYU in 1990 as a Clinical Instructor. He rose through the ranks and was made a tenured Professor in 2005.

Dr. Wisniewski's laboratory focuses on gaining a better understanding of conformational disorders such as Alzheimer’s disease (AD) and prion related disease. He also has an interest in the neuropathology of autism and autism spectrum disorders. This work has led to >240 peer-reviewed publications and has been continuously funded by NIH for >20years. Many of these are highly cited works; Dr. Wisniewski’s h-Index is ~58 (using Web of Science) and ~62 (using Google Scholar).  His manuscripts have >13,000 total citations. Dr. Wisniewski has been a member of numerous NIH study section committees and has given hundreds of invited seminars both nationally and internationally. This work has also produced twelve issued NYU patents and a further 2 patents that are under review. A key contribution was discovering the role of apolipoprotein E in driving amyloid β accumulation in late-onset AD. Dr. Wisniewski's laboratory coined the term “pathological chaperone” to denote the role of apoE in AD, even prior to the discovery of linkage of apoE4 to late-onset AD. This represented the initial recognition of the critical role apolipoprotein E plays in the pathogenesis of AD. Dr. Wisniewski laboratory went on to demonstrate,through a series of papers,that the apoE/Aβ complexes exist in the AD brain and that this interaction plays an important role in the conformational state of Aβ, as well as its clearance. Using the pathological chaperone hypothesis, Dr. Wisniewski has pioneered a novel therapeutic approach to treat AD-related pathology by blocking the binding of Aß and apoE, using Aβ12-28P. This approach has been shown to be highly effective in multiple AD transgenic lines, reducing the amyloid plaque burden and tau related pathology, with resulting cognitive benefits. 

Dr. Wisniewski has also been developing strategies for the prevention of amyloid β accumulation and its removal in AD using non-toxic, highly immunogenic Aβ homologous peptides as “vaccines”. He has uses immunomodulation to ameliorate both amyloid β and tau related pathology concurrently.  This approach induces an immune response specific to the shared pathological conformation of both oligomer/fibrillar Aβ and tau, as well as other amyloid proteins using a non-self immunogen. This is a ground breaking concept in that such an approach could allow for the simultaneous targeting of multiple amyloid prone pathological proteins.  Dr. Wisniewski’s laboratory is also evaluating the potential of innate immunity stimulation as a treatment for AD; with on-going trails of therapy in non-human primates. In addition, Dr. Wisniewski’s laboratorywas the first to document the effectiveness of vaccination in prion disease in vivo using wild type mice and more recently were the first group to effectively use mucosal immunization to prevent prion infection. The Wisniewski lab has generated exciting data in white tailed deer showing that this approach is partially effective for chronic wasting disease (CWD) prevention. CWD is a relatively new prion disease that is epidemic in North America and has the potential to spread to humans, similar to bovine spongiform encephalopathy.  This CWD vaccine represents the first prevention treatment for a prion disease in a species that naturally is at risk for prion infection. In addition the Wisniewski laboratory has developed novel imaging methodologies to detect AD pathology using MRI techniques.

These various studies by Dr. Wisniewski's laboratory have helped direct our greater understanding of abnormal protein accumulation in the brain towards diagnostic and therapeutic interventions.