Minocyline is a
tetracycline derivative with anti-inflammatory, anti-apoptotic, and
anti-oxidant properties.
Therapy has proved useful in some experimental models of both noninfectious and infectious neurological diseases and also in clinical trials in humans, including acute traumatic cervical spinal cord injury. In models of
viral encephalitis, treatment has shown both beneficial and deleterious effects. In
reovirus infection in mice,
minocycline delayed the disease, but did not improve either the morbidity or mortality of the disease. In neuroadapted
Sindbis virus infection of mice,
minocycline prevented disease, but
therapy needed to be given before clinical signs were present in most of the animals. In experimental
rabies in neonatal mice
minocycline aggravated the disease, likely related to anti-inflammatory effects.
Minocycline has also been shown to aggravate disease in a mouse model of
Huntington disease, in a monkey model of
Parkinson disease, and in a mouse model of hypoxic-ischemic
brain injury. Hence, there is experimental evidence of benefit of
minocycline in both infectious and noninfectious neurological diseases, but there is a lack of benefit and harmful effects in other diseases. This may reflect multiple mechanisms of actions that cannot be predicted in a new disease or in an
infection caused by a specific viral agent.
Minocycline therapy is a double-edged sword and this
drug should not be given empirically to patients with acute
viral encephalitis for anticipated
neuroprotective effects. Much more work needs to be done in experimental models in animals as well as in clinical trials. Because patient enrollment in clinical trials on acute
viral encephalitis has proven to be difficult, funding will be a challenge.