"Give with a free hand, but give only your own."
 -- J.R.R. Tolkien The Children of Hurin
Nilotinib -

General Information:

Wikipedia entry: 


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.

Known sources:

Natural sources:


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]

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...




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Updated: July 25, 2012
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