ironjustice
2012-03-03 01:49:02 UTC
The novel multi-target iron chelating-radical scavenging compound M30
possesses beneficial effects on major hallmarks of Alzheimer's
disease.
Antioxid Redox Signal. 2012 Feb 23.
Kupershmidt L, Amit T, Bar Am O, Youdim MB, Weinreb O.
Technion-Eve Topf Center, Rappaport Faculty of Medicine, Haifa,
Israel; ***@tx.technion.ac.il.
Abstract
Aims:
The aim of the present study was to evaluate the therapeutic effect of
the novel neuroprotective multi-target non-toxic, lipophilic, brain
permeable monoamine oxidase inhibitor and iron chelating-radical
scavenging drug, M30, on the neuropathology and deficits of spatial
learning and memory in amyloid precursor protein (APP) and presenilin
1 (PS1) double-transgenic (Tg) Alzheimer's disease (AD) mice.
Results:
Here, we report that systemic treatment of APP/PS1 Tg mice with M30
for 9 months, significantly attenuated cognitive impairments in a
variety of tasks of spatial learning and memory retention, working
memory, learning abilities, anxiety levels, and memory for novel food
and nesting behaviour. Furthermore, we found that M30 reduced cerebral
iron accumulation accompanied by a marked decrease in several AD-like
phenotypes, including cerebral APP levels, amyloid β (Aβ) levels and
plaques, phospho-APP and phospho-tau. Signaling studies revealed that
M30 markedly down-regulated the levels of phosphorylated cyclin-
dependent kinase 5 and increased protein kinase B and glycogen
synthase kinase 3β phosphorylation.
Innovation:
Accumulation and deposition of brain iron is central to various
neuropathological processes in AD, including oxidative stress, amyloid
deposition and tau phosphorylation. Thus, the concept of iron
chelation holds considerable promise as a therapeutic strategy for AD
pathogenesis. Here, for the first time, we demonstrated that when
systemically administered to APP/PS1 Tg mice, our novel
multifunctional iron chelating/radical scavenging compound, M30,
effectively reduced Aβ accumulation and tau phosphorylation, and
attenuated memory deficits.
Conclusions:
These findings suggest that M30 is a potential therapeutic agent for
the prevention and treatment of AD.
PMID:22360429
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possesses beneficial effects on major hallmarks of Alzheimer's
disease.
Antioxid Redox Signal. 2012 Feb 23.
Kupershmidt L, Amit T, Bar Am O, Youdim MB, Weinreb O.
Technion-Eve Topf Center, Rappaport Faculty of Medicine, Haifa,
Israel; ***@tx.technion.ac.il.
Abstract
Aims:
The aim of the present study was to evaluate the therapeutic effect of
the novel neuroprotective multi-target non-toxic, lipophilic, brain
permeable monoamine oxidase inhibitor and iron chelating-radical
scavenging drug, M30, on the neuropathology and deficits of spatial
learning and memory in amyloid precursor protein (APP) and presenilin
1 (PS1) double-transgenic (Tg) Alzheimer's disease (AD) mice.
Results:
Here, we report that systemic treatment of APP/PS1 Tg mice with M30
for 9 months, significantly attenuated cognitive impairments in a
variety of tasks of spatial learning and memory retention, working
memory, learning abilities, anxiety levels, and memory for novel food
and nesting behaviour. Furthermore, we found that M30 reduced cerebral
iron accumulation accompanied by a marked decrease in several AD-like
phenotypes, including cerebral APP levels, amyloid β (Aβ) levels and
plaques, phospho-APP and phospho-tau. Signaling studies revealed that
M30 markedly down-regulated the levels of phosphorylated cyclin-
dependent kinase 5 and increased protein kinase B and glycogen
synthase kinase 3β phosphorylation.
Innovation:
Accumulation and deposition of brain iron is central to various
neuropathological processes in AD, including oxidative stress, amyloid
deposition and tau phosphorylation. Thus, the concept of iron
chelation holds considerable promise as a therapeutic strategy for AD
pathogenesis. Here, for the first time, we demonstrated that when
systemically administered to APP/PS1 Tg mice, our novel
multifunctional iron chelating/radical scavenging compound, M30,
effectively reduced Aβ accumulation and tau phosphorylation, and
attenuated memory deficits.
Conclusions:
These findings suggest that M30 is a potential therapeutic agent for
the prevention and treatment of AD.
PMID:22360429
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk