The NIH’s National Institute of Mental Health is funding
a $60 million effort to find treatments to counteract HIV’s
effects on the human brain. In the early years of the epidemic,
AIDS dementia caused degeneration in some persons
to the level of degeneration in patients with endstage
Alzheimer disease; death typically followed within
6 months. With today’s treatments, the often unpredictable
condition known as neuroAIDS is more subtle
and appears 4 or more years before death. The memory
loss this condition generates can cause patients to forget
their medications and further exacerbate their condition.
Experts speculate that if HIV patients live long enough,
virtually all will experience some neuroAIDS symptoms
(Neergaard L. Associated Press. October 2, 2006).
The NIH-backed research is taking 2 approaches. The
first is to determine which AIDS drugs give the best results
for patients with memory loss. Ron Ellis of the University
of California, San Diego, said that while some
AIDS drugs—such as nevirapine(Drug information on nevirapine), abacavir(Drug information on abacavir), zidovudine(Drug information on zidovudine),
and indinavir(Drug information on indinavir)—can cross the blood-brain barrier, it is not
known whether they can slow brain damage after the
onset of neuroAIDS. Next year, Ellis will lead a study in
which 120 patients will be assigned either to a brain-penetrating
combination or to other drugs.
The second effort will seek to find drugs to protect
nerve cells from inflammation-triggered toxicity. Two
candidate treatments are the epilepsy drug valproic acid
and the manic-depression drug lithium(Drug information on lithium). Both inhibit production
of the enzyme GSK-3b. Too much of this naturally
occurring substance can be poisonous, and HIV damages
the brain by causing an imbalance in the enzyme’s
production. Astudy by Harris Gelbard, a neurologist at
the University of Rochester Medical Center, found indications
that valproic acid might increase brain connections
in neuroAIDS patients.
In addition, Gelbard hopes to launch human studies
of an experimental drug that targets a different inflammation-
producing protein that HIV uses to make brain
cells self-destruct. [CDC HIV/STD/TB Prevention News Update,
Friday, October 6, 2006]
The NIH’s National Institute of Mental Health is funding
a $60 million effort to find treatments to counteract HIV’s
effects on the human brain. In the early years of the epidemic,
AIDS dementia caused degeneration in some persons
to the level of degeneration in patients with endstage
Alzheimer disease; death typically followed within
6 months. With today’s treatments, the often unpredictable
condition known as neuroAIDS is more subtle
and appears 4 or more years before death. The memory
loss this condition generates can cause patients to forget
their medications and further exacerbate their condition.
Experts speculate that if HIV patients live long enough,
virtually all will experience some neuroAIDS symptoms
(Neergaard L. Associated Press. October 2, 2006).
The NIH-backed research is taking 2 approaches. The
first is to determine which AIDS drugs give the best results
for patients with memory loss. Ron Ellis of the University
of California, San Diego, said that while some
AIDS drugs—such as nevirapine(Drug information on nevirapine), abacavir(Drug information on abacavir), zidovudine(Drug information on zidovudine),
and indinavir(Drug information on indinavir)—can cross the blood-brain barrier, it is not
known whether they can slow brain damage after the
onset of neuroAIDS. Next year, Ellis will lead a study in
which 120 patients will be assigned either to a brain-penetrating
combination or to other drugs.
The second effort will seek to find drugs to protect
nerve cells from inflammation-triggered toxicity. Two
candidate treatments are the epilepsy drug valproic acid
and the manic-depression drug lithium(Drug information on lithium). Both inhibit production
of the enzyme GSK-3b. Too much of this naturally
occurring substance can be poisonous, and HIV damages
the brain by causing an imbalance in the enzyme’s
production. Astudy by Harris Gelbard, a neurologist at
the University of Rochester Medical Center, found indications
that valproic acid might increase brain connections
in neuroAIDS patients.
In addition, Gelbard hopes to launch human studies
of an experimental drug that targets a different inflammation-
producing protein that HIV uses to make brain
cells self-destruct. [CDC HIV/STD/TB Prevention News Update,
Friday, October 6, 2006]
