The Oskar Fischer Prize competition has concluded and is no longer accepting inquiries.

Award recipients and their abstracts can be found below.

The Oskar Fischer Prize

According to the World Alzheimer Report 2021 by Alzheimer’s Disease International, an estimated 55 million people worldwide are living with dementia. That population is expected to increase to 78 million by 2030.

To expand the understanding and explanation of Alzheimer’s disease, United States businessman James Truchard gave a $5 million USD gift to The University of Texas at San Antonio (UTSA) College of Sciences to establish the Oskar Fischer Prize. The initiative launched in December 2019, engaging the world’s brightest minds in a comprehensive literature review and taking a new systems approach to the research on Alzheimer’s, building on the work Oskar Fischer started over a century ago.

Submissions from around the world synthesized the breadth of Alzheimer’s disease research to-date and were reviewed by an interdisciplinary committee of advisors. Ten individuals were selected to receive gold, silver and bronze prizes for their papers. Winners were announced June 8, 2022.

The Oskar Fischer Prize Recipients

Congratulations to the winners of the Oskar Fischer Prize! The 10 winners – awarded gold, silver and bronze prizes – synthesized the breadth of Alzheimer’s disease research to-date and provided invaluable perspectives on explanations of the disease. For decades, research has focused on just a few targets. We’ve long been missing pieces of the puzzle to see the complete picture of the disease. These winners brought forth 10 distinct, innovative ideas that look beyond the prevailing theories and could direct future research and treatments. Some of the categories that emerged include: autophagy, lysosome and mitochondria; ApoE and excitation; neural stem cells; and the immune system. Learn more about the winners and their winning explanations below.

Gold Prize Recipients

Carlo Abbate, Ph.D.
IRCCS Fondazione Don Carlo Gnocchi, Istituto Palazzolo
Milan, Italy

  • About Dr. Abbate

    Carlo Abbate, Ph.D., is a senior clinical neuropsychologist and researcher at the IRCCS Fondazione Don Carlo Gnocchi, Istituto Palazzolo in Milan and serves as a consultant neuropsychologist at the Istituto Clinico Quarenghi in San Pellegrino, Bergamo. He has special training in the detection of early signs and symptoms of cognitive decline of dementia. In his clinical practice, he administers about 400 full neuropsychological evaluations each year on patients suspected of cognitive impairment. Along with his clinical practice, his research focuses on mild cognitive impairment, phenotypic (syndromic) variant of Alzheimer’s disease, early and timely dementia diagnosis, and signs and symptoms method in neuropsychology. He has published around 60 scientific articles on dementia. Prior to his current role, he previously worked in the Geriatric Unit of the Fondazione Ca’ Granda, Ospedale Maggiore Policlinico in Milan for about 20 years. Dr. Abbate graduated with a bachelor’s degree in Experimental Psychology and a master’s degree in Neuropsychology of Acquired Cognitive Disorders from the University of Padua, Italy. He also has a doctorate in Physiopathology of Aging from the University of Milan.
  • Abstract

    Alzheimer’s disease starts in neural stem cells (NSCs) in the niches of adult neurogenesis. All primary factors responsible for pathological tau hyperphosphorylation are inherent to adult neurogenesis and migration. However, when amyloid pathology is present, it strongly amplifies tau pathogenesis. Indeed, the progressive accumulation of extracellular amyloid-β deposits in the brain triggers a state of chronic inflammation by microglia. Microglial activation has a significant pro-neurogenic effect that fosters the process of adult neurogenesis and supports neuronal migration. Unfortunately, this “reactive” pro-neurogenic activity ultimately perturbs homeostatic equilibrium in the niches of adult neurogenesis by amplifying tau pathogenesis in AD. This scenario involves NSCs in the subgranular zone of the hippocampal dentate gyrus in late-onset AD (LOAD) and NSCs in the ventricular-subventricular zone along the lateral ventricles in early-onset AD (EOAD), including familial AD (FAD). Neuroblasts carrying the initial seed of tau pathology travel throughout the brain via neuronal migration driven by complex signals and convey the disease from the niches of adult neurogenesis to near (LOAD) or distant (EOAD) brain regions. In these locations, or in close proximity, a focus of degeneration begins to develop. Then, tau pathology spreads from the initial foci to large neuronal networks along neural connections through neuron-to-neuron transmission.