Minocycline - Wikipedia, the free encyclopedia

Anti-Inflammatory and Neuroprotective

Current research is examining the possible neuroprotective and anti-inflammatory effects of minocycline against progression of a group of neurodegenerative disorders including Multiple Sclerosis (MS), Rheumatoid Arthritis (RA), Amyotrophic Lateral Sclerosis (ALS), Huntington's Disease, and Parkinsons disease,^[1] amongst others nuerodegenerative diseases. ^[2][3][2]

The neuroprotective action of minocycline may include its inhibitory effect on 5-lipoxygenase, ^[5] an inflammatory enzyme associated with brain aging and is being studied for use in Alzheimers patients.^[5] It also has been used as a "last ditch" treatment for toxoplasmosis in AIDS patients. Minocycline is neuroprotective in mouse models of amyotrophic lateral sclerosis (ALS) and Huntington's disease and has been recently shown to stabilize the course of Huntington's disease in humans over a 2-year period.

As an anti-inflammatory, minocycline inhibits apoptosis (cell death) via attenuation of TNF-alpha, downregulating pro-inflammatory cytokine output. This effect is mediated by a direct action of minocycline on the activated T cells and on microglia, which results in the decreased ability of T cells to contact microglia which impairs cytokine production in T cell-microglia signal transduction.^[3]Minocycline also inhibits microglial activation, through blockade of NF-kappa B nuclear translocation.

It is thought that minocycline exerts neuroprotective effects independent of its anti-inflammatory properties. ^[4]

A recent study reported the impact of the antibiotic minocycline on clinical and magnetic resonance imaging (MRI) outcomes and serum immune molecules in MS patients over 24 months of open-label minocycline treatment. Despite a moderately high pretreatment relapse rate in patients in the study prior to treatment, no relapses occurred between months 6 and 24. The only patient with gadolinium-enhancing lesions on MRI at 12 and 24 months was on half-dose minocycline. Levels of interleukin-12 (IL-12), which at high levels might antagonize the proinflammatory IL-12 receptor, were elevated over 18 months of treatment, as were levels of soluble vascular cell adhesion molecule-1 (VCAM-1). The activity of matrix metalloproteinase-9 was decreased by treatment. Clinical and MRI outcomes in this study were supported by systemic immunological changes and call for further investigation of minocycline in MS.^{[5] [6][7][8]}

http://en.wikipedia.org/wiki/Minocycline