Chronic Microglial Activation

Research in the Block Laboratory strives to understand how and why microglia become chronically activated to drive central nervous system (CNS) disease.  Our research explores how events in the periphery (outside of the brain)  in addition to events occurring directly in the brain parenchyma can initiate and augment chronic microglia-mediated neuropathology.

Neurotoxic Reactive Microgliosis

Reports indicate that microglial activation and progressive neuron damage can continue years after the initial “stimulus”, long after the instigating toxicant or injury is gone.

Examples of chronic/persistent microglial activation: Neurotrauma (human & monkey), Neurotrauma (mice), MPTP human, & MPTP monkeys.


The persistent neurotoxic microglial response (reactive microgliosis) is implicated in the progressive nature of diverse neurodegenerative diseases (Block et al., 2007, Nature Reviews Neuroscience).

Previous work from our laboratory has shown that dopaminergic neurons may be particularly vulnerable to reactive microglisosis and that mu calpain is an important pro-inflammitory neuron injury signal that activates microglia (Levesque et al., Brain, 2010).

Current Research

Ongoing research investigates the underlying mechansims responsible for why microglia fail to resolve the pro-inflammatory response and become persistently toxic. In addition to Parkinson’s disease, we are now perusing new interests and mechanisms in Multiple Sclerosis and Neurotrauma.