Ageing, neuroinflammation and neurodegeneration.

Abstract

During ageing, different iron complexes accumulate in specific brain regions which are associated with motor and cognitive dysfunction. In neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease, changes in local iron homoeostasis result in altered cellular iron distribution and accumulation, ultimately inducing neurotoxicity. The use of iron chelators which are able to penetrate the blood brain barrier and reduce excessive iron accumulation in specific brain regions have been shown to reduce disease progression in both Parkinson's disease and Friedreich's Ataxia. Neuroinflammation often occurs in neurodegenerative diseases, which is mainly sustained by activated microglia exhibiting the M1 phenotype. Such inflammation contributes to the disease progression. Therapeutic agents which reduce such inflammation, e.g. taurine compounds, may ameliorate the inflammatory process by switching the microglia from a M1 to a M2 phenotype.

• Authors: Roberta J Ward, David T Dexter, Robert R Crichton
• Journal: Frontiers in bioscience (Scholar edition) (Front Biosci (Schol Ed)) Vol. 7 Issue 1 Pg. 189-204 (06 01 2015) ISSN: 1945-0524 [Electronic] Singapore
• PMID: 25961695 (Publication Type: Journal Article, Review)

Chemical References

• Iron Chelating Agents
• Iron

Topics

• Aging (metabolism, pathology)
• Animals
• Brain (metabolism, pathology)
• Humans
• Iron (metabolism)
• Iron Chelating Agents
• Neurodegenerative Diseases (metabolism, pathology)
• Neurogenic Inflammation (metabolism, pathology)