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Sex
hormones as neuroprotective agents in a transgenic mouse model of Huntington's
disease
Principal
Investigator: Claire-Anne Gutekunst, PhD
Emory University Department of Neurology
Investigator:
Brian Ciliax, PhD
Emory University Department of Neurology
Investigator:
David Edwards, PhD
Emory University Department of Neurology
Background
Huntington's disease (HD) is a dominant inherited neurodegenerative disorder
that affects 1 in 10,000 in the U.S. with about 4 times more at risk for
the disease. HD causes motor and cognitive dysfunctions, the degeneration
of striatal, cortical and hypothalamic neurons in the brain, and death
of its victim within 15-20 years. Although the HD mutation has been identified,
the mechanism by which the abnormal trinucleotide repeat expansion leads
to neuronal cell death and the specific HD neuropathology remains unclear.
Mutant huntingtin forms aggregates in the nucleus, perikarya and processes
of neurons in humans and in animal models of HD that also contain the
transcriptional coactivator CREB binding protein (CBP). CBP recruitment
into polyglutamine-containing aggregates disrupts the protein normal function.
CBP enhances the transactivation of many transcription factors, including
the androgen receptor (AR). It is possible that perturbation of CBP-AR
interaction contributes to the process leading to cell death.
Study
We hypothesize that a loss of CBP function following its recruitment into
aggregates in HD might be compensated by increased levels of testosterone
(T). Both androgen and estrogen have been shown to have neuroprotective
effects. We will investigate the effect of supplementation of sex hormones
via subcutaneous pellets on the course of the behavioral phenotype and
brain neurophathology in HD171-82Q mice. We will also investigate the
effect of gonadectomy on these same parameters. From these studies we
will learn the role sex hormones play in the neuropathology of HD and
determine whether these alternative therapies should be consider for HD.
A
Controlled Pilot Study of the Effects of Neuromuscular Massage Therapy
in Patients with Parkinson's Disease
Principal
Investigator: Laurie Craig, M.S.
Director of Education, Atlanta School of Massage Therapy
Investigator:
Leticia Allen, L.M.T.
President, Atlanta School of Massage Therapy
Investigator:
Anna Svircev, B.S.
Graduate Student in Public Health, Emory University
Background
Neuromuscular massage therapy (NMT) and deep tissue (DT) massage therapy
have been shown to benefit selected neuromuscular disorders by reducing
painful muscular trigger points and muscle tension. Parkinson's disease
(PD) is a muscular disorder characterized by muscular tension, rigidity,
bradykinesia and tremor. NMT and DT massage therapies are based on the
premises that through the application of deep focal pressure (NMT) and
broad repetitive strokes along muscular tissue planes (DT), significant
reduction of these symptoms can be achieved.
Study
NMT may ameliorate
the symptoms of PD, however there is only limited literature and no controlled
studies to support this view. Based on this limited literature and our
own anecdotal experience, we hypothesize that NMT can improve the signs
and symptoms of PD. Furthermore we postulate that touch is fundamental
to this improvement.
In this study, we will:
(1) examine the magnitude and variability of the acute effects of NMT
on gross and fine motor function in patients with moderately advanced
PD using standard validated clinical measures; (2) examine the duration
of this effect, and thus determine the minimum dose of massage therapy
necessary to have a sustained clinical benefit; and (3) examine techniques
for controlling the potential non-musculoskeletal effects of massage therapy
on important contributors to Quality of Life (QOL) in PD such as anxiety
and depression.
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