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Alessandro Didonna

Researcher at University of California, San Francisco

Publications -  36
Citations -  827

Alessandro Didonna is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Neurodegeneration & Experimental autoimmune encephalomyelitis. The author has an hindex of 15, co-authored 29 publications receiving 603 citations. Previous affiliations of Alessandro Didonna include International School for Advanced Studies & Northwestern University.

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Giant axonal neuropathy-associated gigaxonin mutations impair intermediate filament protein degradation.

TL;DR: It is demonstrated that gigaxonin was responsible for the degradation of vimentin IFs and proteasome inhibition by MG-132 reversed the clearance of IF proteins in cells overexpressing gigax onin, demonstrating the involvement of the proteasomal degradation pathway.
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The promise and perils of HDAC inhibitors in neurodegeneration

TL;DR: The potential benefits along with the risks of targeting HDACs in light of what the authors currently know about HDAC activity in the brain are reviewed.
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The role of neurofilament aggregation in neurodegeneration: lessons from rare inherited neurological disorders

TL;DR: A number of rare disorders caused by mutations in genes that encode NFs or regulate their metabolism have been discovered and are providing novel insights into the role of NF aggregation in the more common neurological disorders.
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Hyperpolarized 13C MR metabolic imaging can detect neuroinflammation in vivo in a multiple sclerosis murine model

TL;DR: This study showed that a new metabolic imaging method, namely 13C magnetic resonance spectroscopic imaging (MRSI) of hyperpolarized pyruvate, can detect increased lactate production from proinflammatory MPs, a mechanism mediated by pyruVate dehydrogenase kinase 1 upregulation, in a preclinical model of multiple sclerosis.
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Genetic determinants of risk and progression in multiple sclerosis

TL;DR: The biggest challenge for the next era of MS research will consist in identifying and characterizing the molecular mechanisms and the cellular pathways in which these risk variants play a role.