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- Suhayl Dhib-Jalbut, Douglas L Arnold, Don W Cleveland, Mark Fisher, Robert M Friedlander, M Maral Mouradian, Serge Przedborski, Bruce D Trapp, Tony Wyss-Coray, and V Wee Yong.
- UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ 08901, and The Cleveland Clinic, OH, USA. jalbutsu@umdnj.edu
- J. Neuroimmunol. 2006 Jul 1; 176 (1-2): 198-215.
AbstractMultiple sclerosis is considered a disease of myelin destruction; Parkinson's disease (PD), one of dopaminergic neuron depletion; ALS, a disease of motor neuron death; and Alzheimer's, a disease of plaques and tangles. Although these disorders differ in important ways, they also have common pathogenic features, including inflammation, genetic mutations, inappropriate protein aggregates (e.g., Lewy bodies, amyloid plaques), and biochemical defects leading to apoptosis, such as oxidative stress and mitochondrial dysfunction. In most disorders, it remains uncertain whether inflammation and protein aggregation are neurotoxic or neuroprotective. Elucidating the mechanisms that orchestrate neuronal diseases should facilitate development of neuroprotective and neurorestorative strategies.
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