a couple of links to neat stuff last 12 months.
Ray Truant proved a new direct link at micro-level between Alzheimer’s &
Huntington’s. HD cure should have powerful impact on Alzheimer’s.
teams from Calgary & Hamilton have just reversed effect of HD in mice . . .
A few years back did this another way, but finally got this HUGE breakthrough.
This hit all the daily newspapers, often page one, up here. Clinical trials for
people are being talking about in the next year or two. (already fast-tracked
here by our federal government)
Hope has been involved in our own small way in the funding of much of this work.
have recently approved 2 grants:
Simonetta Sipione (of the latter breakthrough) – University of Alberta – 2
years – $75K x 2= $150,000.00
Lynn Raymond – UBC (scene of first reversal) – 2 years – $59,820.00 +
$58,820.00 = $118,640.00
· At this moment we have a shortfall of $65,500 in year after next to meet
the second year of these two commitments.
(nice to have exact goals to be heading towards . . . ;-))
Below; a more extended summary, and below that the links.
I just want to make sure the Cigar PEG members know that not only has
their money had huge, direct impact. But that it will be having more in the
weeks ahead. For Huntington’s, and for Alzheimer’s as well.
Thanks to you, and to all for all they do!
summary from the CEO of the Huntington’s Society:
Promising treatment for Huntington’s disease
Treatment of Huntington’s disease (HD) mice with a naturally occurring lipid
known as GM1 restores normal motor behavior to symptomatic animals, a study
HD is a heritable neurodegenerative disorder caused by a mutant
form of the huntingtin protein. Alba Di Pardo and colleagues investigated
the therapeutic potential of restoring levels of GM1, which was recently
found to be reduced in Huntington’s disease. The authors infused GM1 into
the brains of 5-month old HD mice, which already showed severe motor
impairment. Within two weeks of GM1 administration, treated HD mice
performed as well as wild-type animals on challenging tests of motor
abilities, such as walking along a narrow beam and crossing a horizontal
ladder with an irregular rung pattern.
GM1 treatment also restored normal levels of an early protein marker for
neuronal dysfunction in HD, indicating possible neuroprotective changes in
the brain. The authors found that the therapeutic effects of GM1 are associated
with the induction of huntingtin phosphorylation—a protective modification of the
mutant huntingtin protein that reduces the protein’s toxicity.
The findings may have significant implications for HD patients since GM1’s safety
has already been established in clinical trials of GM1 for the treatment of other
neurological conditions, according to the authors.
Article #11-14502: “Ganglioside GM1 induces phosphorylation of mutant
huntingtin and restores normal motor behavior in Huntington’s disease mice,”
by Ray Truant, and Simonetta Sipione Alba Di Pardo, Vittorio Maglione, Melanie Alpaugh,
Melanie Horkey, Randy S. Atwal, Jenny Sassone, Andrea Ciammola, Joan S. Steffan, Karim Fouad,
CEO & Executive Director
Huntington Society of Canada