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Minocycline, a tetracycline derivative,
prevented degeneration in dopamine-producing brain
cells in mice that were made to have a Parkinson's-like disease.
Parkinson's is marked by the destruction of brain cells that
produce dopamine, a chemical that is a key regulator of muscle
movement.
The brain damage his team induced in
the study mice certainly doesn't mimic the exact cause or
course of Parkinson's disease.
Moreover, the animals required very high
doses of oral minocycline for it to protect the brain -- doses
that may not be "achievable" in patients. If this
research can be extended to humans, a better approach would
likely be to develop a different tetracycline that "gets
into the brain better.
Parkinson's disease is a motor system
disorder in which patients experience tremors, muscle rigidity,
impaired movement, and problems with balance and coordination.
Treatment includes drugs that replace the brain's dwindling
supply of dopamine, but there is no cure for the progressive
loss of dopamine-producing brain cells.
The researchers treated mice with MPTP,
a toxic chemical that induces parkinsonian symptoms in animals
and humans. Groups of mice were treated with minocycline before,
during and after receiving MPTP. Some mice did not receive
the antibiotic.
The investigators found that at high
doses, the drug was able
to protect many dopamine cells from damage when it was given
either before or after MPTP.
Similarly, the researchers note, a recent
study showed that minocycline delayed death in mice made to
show characteristics of Huntington's disease, a genetic disorder
that is also marked by brain cell degeneration.
Minocycline may prevent dopamine-cell
damage by blocking the action of nitric oxide (NO) in the
brain. Some research has suggested that the release of NO
from activated brain cells called glial cells is involved
in the degeneration seen in Parkinson's. This remains only
speculation, however.
Whatever the reason, minocycline seems
to have "neuroprotective effects quite apart from its
antibiotic properties.
Proceedings
of the National Academy of Sciences December 4, 2001;98:14669-14674
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