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Michelle L. Block

Researcher at Virginia Commonwealth University

Publications -  55
Citations -  15639

Michelle L. Block is an academic researcher from Virginia Commonwealth University. The author has contributed to research in topics: Microglia & Neurotoxicity. The author has an hindex of 40, co-authored 54 publications receiving 13736 citations. Previous affiliations of Michelle L. Block include Indiana University & National Institutes of Health.

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Microglia-mediated neurotoxicity: uncovering the molecular mechanisms

TL;DR: Overactivated microglia can be detected using imaging techniques and therefore this knowledge offers an opportunity not only for early diagnosis but, importantly, for the development of targeted anti-inflammatory therapies that might slow or halt the progression of neurodegenerative disease.
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Systemic LPS Causes Chronic Neuroinflammation and Progressive Neurodegeneration

TL;DR: It is demonstrated that through TNFα, peripheral inflammation in adult animals can activate brain microglia to produce chronically elevated pro‐inflammatory factors and induce delayed and progressive loss of DA neurons in the SN, providing valuable insight into the potential pathogenesis and self‐propelling nature of Parkinson's disease.
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Microglia and inflammation-mediated neurodegeneration: Multiple triggers with a common mechanism

TL;DR: Evidence supports that the unregulated activation of microglia in response to environmental toxins, endogenous proteins, and neuronal death results in the production of toxic factors that propagate neuronal injury.
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Aggregated α-synuclein activates microglia: a process leading to disease progression in Parkinson’s disease

TL;DR: The results suggest that nigral neuronal damage, regardless of etiology, may release aggregated α‐synuclein into substantia nigra, which activates microglia with production of proinflammatory mediators, thereby leading to persistent and progressive nigral neurodegeneration in PD.
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Air pollution: mechanisms of neuroinflammation and CNS disease

TL;DR: Recent findings detailing the mechanisms through which air pollution reaches the brain and activates the resident innate immune response to become a chronic source of pro-inflammatory factors and ROS, culminating in CNS disease are summarized.