Polymerencapsulated Cells To Deliver Neurotrophic Factors In Animal Models Of Hd

HD is an inherited, progressive neurological disorder characterized by a severe degeneration of basal ganglia neurons, particularly the intrinsic neurons of the striatum. Accompanying the pathological changes is a progressive dementia coupled

Cell and Gene Therapy for CNS Diseases

Cell and Gene Therapy for CNS Diseases

Figure 7 (a) Expression vector containing the NGF gene. (b) NGF levels, as determined by ELISA, in unencapsulated (top) and encapsulated (bottom) BHK cells. The in vivo levels were determined from devices 3 months following explant from rodent striatum. (c) The biological activity of the NGF from encapsulated BHK cells is shown in phase-contrast photomicrographs of PC12 cells that exhibit exytensive neurite processes. Original magnification, 25 um.

Figure 7 (a) Expression vector containing the NGF gene. (b) NGF levels, as determined by ELISA, in unencapsulated (top) and encapsulated (bottom) BHK cells. The in vivo levels were determined from devices 3 months following explant from rodent striatum. (c) The biological activity of the NGF from encapsulated BHK cells is shown in phase-contrast photomicrographs of PC12 cells that exhibit exytensive neurite processes. Original magnification, 25 um.

with uncontrollable movements and abnormal postures. From the time of onset, an intractable course of mental deterioration and progressive motor abnormalities begins with death usually occurring within 15 to 17 years. Overall, the prevalence rate of HD in the United State is approximately 50 per 1,000,000 (87). At present, there is no treatment that effectively addresses the behavioral symptoms or slows the inexorable neural degeneration in HD.

Intrastriatal injections of excitotoxins such as quinolinic acid (QA) have become a useful model of HD and can serve to evaluate novel therapeutic strategies aimed at preventing, attenuating, or reversing neuroanatomical and behavioral changes associated with HD (88-91). The use of trophic factors in a neural protection strategy may be particularly relevant for the treatment of HD. Unlike other neurodegenerative diseases, genetic screening can identify virtually all individuals at risk who will ultimately suffer from HD. This provides a unique opportunity to design treatment strategies to intervene prior to the onset of striatal degeneration. Thus, instead of replacing neuronal systems, which have already undergone extensive neuronal death, trophic factor strategies could be designed to support host systems destined to die at later time in the patient's life.

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