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-- J.R.R. Tolkien The Children of Hurin
- Nilotinib -
General Information:
Names:
Wikipedia entry:
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Observations:
Nilotinib,
is approved by the FDA to treat chronic myelogenous leukemia
(CML), a cancer. It forces cancer cells into autophagy. In low doses, it is
thought to turn on just enough autophagy in neurons that the
cells would clear malfunctioning proteins, but not damage the
cell's internal organelles.
Another CML
drug, bosutinib, may also be beneficial.
The sugar trehalose is also though to promote
autophagy, and has been reported to be benefical for people with
Huntington's disease.
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Known sources:
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Natural sources:
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References:
Nilotinib reverses
loss of dopamine neurons and improves motor behavior via
autophagic degradation of α-synuclein in Parkinson's disease
models.
Hebron ML, Lonskaya I, Moussa CE.
Hum Mol Genet. 2013 May 10. [Epub ahead of print]
Source: Department of Neuroscience, Laboratory for Dementia and
Parkinsonism, Georgetown University Medical Center, Washington,
DC 20057, USA.
Abstract: Parkinson's disease is a movement disorder
characterized by death of dopaminergic substantia nigra (SN)
neurons and brain accumulation of α-synuclein. The tyrosine
kinase Abl is activated in neurodegeneration. Here, we show that
lentiviral expression of α-synuclein in the mouse SN leads to
Abl activation (phosphorylation) and lentiviral Abl expression
increases α-synuclein levels, in agreement with Abl activation
in PD brains. Administration of the tyrosine kinase inhibitor
nilotinib decreases Abl activity and ameliorates autophagic
clearance of α-synuclein in transgenic and lentiviral gene
transfer models. Subcellular fractionation shows accumulation of
α-synuclein and hyper-phosphorylated Tau (p-Tau) in autophagic
vacuoles in α-synuclein expressing brains, but nilotinib
enhances protein deposition into the lysosomes. Nilotinib is
used for adult leukemia treatment and it enters the brain within
US Food and Drug Administration approved doses, leading to
autophagic degradation of α-synuclein, protection of SN neurons
and amelioration of motor performance. These data suggest that
nilotinib may be a therapeutic strategy to degrade α-synuclein
in PD and other α-synucleinopathies.
PMID: 23666528 [PubMed]
http://www.ncbi.nlm.nih.gov/pubmed/23666528
Cancer Drug Prevents
Build-Up of Toxic Brain Protein
May 10, 2013 — Researchers at Georgetown University Medical
Center have used tiny doses of a leukemia drug to halt
accumulation of toxic proteins linked to Parkinson's disease in
the brains of mice. This finding provides the basis to plan a
clinical trial in humans to study the effects...
http://www.sciencedaily.com/releases/2013/05/130510075623.htm
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Updated: July 25, 2012
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