Neuroprotective Effects of Minocycline: Expanding its Use in Clinical Medicine
Minocycline (MCN) exhibits significant neuroprotective effects 1 in many neurological conditions.
MCN attenuates disease progression in Parkinson’s disease. It mediates this role in part by suppressing the nuclear translocation of nuclear factor-κB. At the same time, MCN has a negative impact on the number of activated microglia. Leem et al2 have recently reported that this in turn restricts prothrombin kringle-2–induced neurotoxicity against dopaminergic neurons. In addition, MCN decreases p38 mitogen-activated protein kinase phosphorylation. This is accompanied by downregulation of cleaved intracranial atherosclerotic disease levels.3 Thus, MCN attenuates intracranial oxidative stress thereby protecting dopaminergic neurons.
MCN also exhibits a neuroprotective effect against Alzheimer disease. It mediates this role by attenuating tau cleavage by caspase-3. In addition, Ferretti et al4 have recently demonstrated that MCN has an inhibitory effect on β-site amyloid precursor protein cleaving enzyme 1 levels. Concurrently, MCN restricts “eukaryotic translation initiation factor-2 alpha” phosphorylation. At the same time, MCN accentuates Aβ fibrils phagocytosis thereby decelerating intracranial neuronal changes seen in Alzheimer disease.5
The above examples clearly illustrate the significant neuro-protective effects of MCN.