Draining Toxins from Alzheimer's Disease Patients Stabilizes Cognitive Decline
May / June 2005
Draining toxins from cerebral spinal fluid (CSF) in the
brain of Alzheimer's disease (AD) patients appears
to stabilize the cognitive disease. Penn
pharmacologists participated in a pilot study demonstrating
these results and the work appears in the August 2004 issue
of the Journal of Alzheimer’s Disease.
The study tested the hypothesis that with aging, and in
particular with AD, there is a reduced clearance of some
toxic compounds in the cerebral spinal fluid that surrounds
the brain. If these compounds are cleared, then the clinical
outcome of the disease could improve.
The leading cause of dementia, AD advances at varying rates
and initially affects areas of the brain that control memory
and thinking skills. The build-up of some toxins known as
isoprostanes, which specifically reflect oxidative damage,
and misfolded proteins are common in the brains of
AD patients. The ever-slowing capacity to clear this build-up
of toxins causes the death of cells involved in memory and
language.
The small study included a control group and eight participants
who were implanted with a low-flow ventriculoperitoneal shunt
designed to increase flow of CSF and improve clearance of
neurotoxins from the fluid bathing the brain. All of the
study participants had medium-stage AD. The microns-wide
shunt, or catheter, was placed subcutaneously in a space
at the base of the cerebellum.
It runs under the skin to the peritoneum and the excess toxins
are eliminated in the urine.
The shunt is put in once, drains
continuously, and is cleaned out periodically by a neurologist.
Additionally, the normal components of CSF like glucose
and immunoglobulins did not change after the shunt was placed
in patients. Currently, under evaluation by the FDA as
an
investigational device, the shunt has a selective capacity
to filter out toxins of a specific molecular weight and
size, in this case isoprostanes.
After 12 months, the study participants’ isoprostanes
were reduced by about 50 percent and their cognitive ability
remained stable. However, patients in the control group had
the typical 20 percent decline in cognitive ability at 12
months. All participants continued taking their standard
anti-Alzheimer’s medication throughout the study.
“Currently no therapy has proven to work long-term
for AD. This device is a promising, new opportunity that,
in the future, may be implanted in patients with AD at an
earlier stage of the disease. If a primary care physician
has a patient with a memory disorder, the patient should
be referred to a memory disorder clinic or neurologist— the
earlier the better,” says Domenico Pratico, MD, associate
professor of pharmacology at the University of Pennsylvania
School of Medicine. This research is one of many Penn studies
focused on the cause and treatment of AD.
“Although not a cure for AD, we demonstrated that
the clearance of this compound is possible and in so doing
we can improve the clinical picture of the patient,” adds
Dr. Pratico.
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