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231.
Huntington''s disease (HD) is a complex and severe disorder characterized by the gradual and the progressive loss of neurons, predominantly in the striatum, which leads to the typical motor and cognitive impairments associated with this pathology. HD is caused by a highly polymorphic CAG trinucleotide repeat expansion in the exon-1 of the gene encoding for huntingtin protein. Since the first discovery of the huntingtin gene, investigations with a consistent number of in-vitro and in-vivo models have provided insights into the toxic events related to the expression of the mutant protein. In this review, we will summarize the progress made in characterizing the signaling pathways that contribute to neuronal degeneration in HD. We will highlight the age-dependent loss of proteostasis that is primarily responsible for the formation of aggregates observed in HD patients. The most promising molecular targets for the development of pharmacological interventions will also be discussed. 相似文献
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S. Sumbul M. S. Khan B. Bano 《Biochemistry (Moscow) Supplemental Series B: Biomedical Chemistry》2009,3(3):259-265
Cystatins are thiol proteinase inhibitors ubiquitously present in the mammalian body. In brain, they prevent unwanted proteolysis
and are involved in several neurodegenerative diseases. Under physiological conditions nitric oxide can be found in almost
all the tissues, but under pathological conditions NO has damaging effects. Its increased concentration, under various neural
diseases leads to cell damage through formation of highly reactive peroxynitrite. Our present study was designed to investigate
the protective effect of curcumin against NO induced damage of HM-GBC. NO caused intensive structural and functional damage
of HM-GBC, resulting in 89% loss of its antiproteolytic activity after 2 h of incubation. Structural damage occurs in the
form of protein degradation. Curcumin significantly protected HM-GBC against this damage. This suggests that curcumin has
a significant potential in the treatment of diseases caused by nitrogen free radicals and this potential must be further explored
for the development of novel drugs.
This text was submitted by the authors in English. 相似文献
235.
Human clinical and psychophysical observations suggest that the taste
system is able to compensate for losses in peripheral nerve input, since
patients do not commonly report decrements in whole mouth taste following
chorda tympani nerve damage or anesthesia. Indeed, neurophysiological data
from the rat nucleus of the solitary tract (NST) suggests that a release of
inhibition (disinhibition) may occur centrally following chorda tympani
nerve anesthesia. Our purpose was to study this possibility further. We
recorded from 59 multi- and single- unit taste-responsive sites in the rat
NST before, during and after recovery from chorda tympani nerve anesthesia.
During anesthesia, average anterior tongue responses were eliminated but no
compensatory increases in palatal or posterior tongue responses were
observed. However, six individual sites displayed increased taste
responsiveness during anesthesia. The average increase was 32.9%.
Therefore, disinhibition of taste responses was observed, but infrequently
and to a small degree in the NST At a subset of sites, chorda
tympani-mediated responses decreased while greater superficial
petrosal-mediated responses remained the same during anesthesia. Since this
effect was accompanied by a decrease in spontaneous activity, we propose
that taste compensation may result in part by a change in signal-to-noise
ratio at a subset of sites.
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