Journal
MOLECULAR NEUROBIOLOGY
Volume 56, Issue 3, Pages 2202-2210Publisher
SPRINGER
DOI: 10.1007/s12035-018-1227-1
Keywords
Diabetes; Axonal transport; Cytoskeleton; Kinesin; Dynein; Neurodegeneration
Categories
Funding
- Foundation for Science and Technology [PEst UID/NEU/04539/2013]
- COMPETE-FEDER [POCI-01-0145-FEDER-007440]
- Centro 2020 Regional Operational Programme [CENTRO-01-0145-FEDER-000008]
- Foundation for Science and Technology, Portugal [SFRH/BPD/86830/2012]
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Diabetes mellitus is a chronic disease with numerous complications that severely impact on the quality of life of patients. Different neuropathies may arise as complications associated with the nervous system, both peripherally and at the central level. The mechanisms behind these neuronal complications are far from being clarified, but axonal transport impairment, a vital process for neuronal physiology, has been described in the context of experimental diabetes. Alterations in neuronal cytoskeleton and motor proteins, deficits in ATP supply or neuroinflammation, as processes that disturb the effective transport of cargoes along the axon, were reported as putative causes of axonal impairment, ultimately leading to axonal degeneration. The main goal of the present review is to reunite the main studies in the literature exploring diabetes-induced alterations likely involved in axonal transport deficits, and call the attention for the uttermost importance of further exploring the field. Understanding the mechanisms underlying neuronal deficits in diabetes is crucial for the development of new therapeutic strategies to prevent neuronal degeneration in diabetes and related neuropathies.
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