Tel Aviv University
Neurobiology
Prof. Dan Frenkel is head of neuroimmunology laboratory at the department of neurobiology at Tel Aviv University. His laboratory research focus is on glial-neuronal cell interactions to clarify their role in neurological diseases, both in culture and in animal models such as multiple sclerosis, Alzheimer’s disease and Parkinson’s disease. His lab combines approaches such as molecular biology as well as immunological approaches to shed light on the genes and proteins involved in glial cell function, in particular microglia and astrocyte. They have developed novel approaches to isolate adult microglia and astrocytes from mice and to investigate their genetic and proteins profile that relate to pathological condition during aging. Furthermore, they aim define the link between glia function to cognition using different behavioral tests. He was awarded career development award for an outstanding young scientist from the Human Frontier Science Program Organization for studying reactive microglia in Alzheimer’s disease. In 2016 he was awarded Mary K. Iacocca Visiting Faculty Fellowship and spent a year as visiting scientist at Joslin Diabetes Center, Harvard Medical School aiming to study the link between diabetes to neuroinflammation. He has been published in an array of scientific journals including the Journal of clinical investigation, Nature Annals of Neurology, the Proceeding National Academy of Science, Nature communication, FASEB, Neurobiology of Aging, and Neurobiology of disease. He has 4 granted patents to treat neurodegenerative diseases.

Presenter of 1 Presentation

PRE-RECORDED: METABOLIC CHANGES IN MICROGLIA AND THEIR EFFECT ON NEUROTOXICITY IN PARKINSON'S DISEASE

Session Type
SYMPOSIUM
Date
Thu, 17.03.2022
Session Time
02:45 PM - 04:45 PM
Room
ONSITE: 113
Lecture Time
04:15 PM - 04:30 PM

Abstract

Abstract Body

Parkinson's disease (PD) , a neurodegenerative disease, is associated with impairment with motor activity and rigidity. The genetic risks of the disease is reported to be between 5 and 10%. It was suggested that activated microglia may play a role in neurotoxicity to dopaminergic neurons (Lazdon et al JNC 2019). We found that reduction in DJ-1 protein ( found in PD patients) in microglia increase both their pro-inflammatory profile and neurotoxicity. Autophagy is an important mechanism for the degradation of intracellular proteins and organelles. We discovered that impaired DJ-1 microglia exhibit an impaired autophagy-dependent degradation of p62 and LC3 proteins, an important protein in the autophagy flux. We discovered that impaired autophagy affects the ability of DJ-1 microglia to uptake αSyn. Further research suggests that αSyn affects microglia metabolism both in vitro and in vivo, leading to their neurotoxic properties. Targeting those metabolic changes in microglia may lead to new therapeutic avenues in the disease.

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