A cancer drug could reportedly help protect brain cells from the effects of Alzheimer’s disease according new research findings. That’s due to the fact that the malfunction of a key brain protein called tau is the likely culprit behind Alzheimer’s disease and other forms of dementia.
Neurons, those highly specialized nerve cells in the brain, appear to die when tau malfunctions and fails to clear the cells of unwanted and toxic proteins, explained Charbel Moussa, head of the Laboratory for Dementia and Parkinsonism at Georgetown University School of Medicine, in Washington, D.C. This means drugs that replace the function of tau in these brain cells are likely to slow the progression of Alzheimer’s, he said.
“For a very long time, we believed, for almost 100 years, that [amyloid-beta] plaques are the main culprit in Alzheimer’s disease,” the study’s senior investigator, Moussa explained. “This study shows it’s another protein, a very, very important one, called tau, is basically the main guilty one.”
Inside a brain cell, tau supplies a structure, some thing akin to a train track, which enables the cell to dispose of accumulations of unwanted toxic proteins. If tau stops functioning, possibly from ageing or from errant genes, the cell is unable to rid itself of the toxins. Contrary to previously belief, it is the protein the cells can’t dispose of and that remains inside neurons that causes them to die, not the plaques that create outside of the cells, the researchers say.
Tests on the brain cells of mice revealed that removing all tau impaired the neurons’ ability to clear out amyloid beta, according to findings published in the journal Molecular Neurodegeneration. But if researchers reintroduced tau into brain cells, the neurons were better able to remove accumulated amyloid beta from the cells. Moussa said his study suggests the remaining amyloid beta inside the neuron destroys the cells, not the plaques that build up outside. The mouse experiments also showed that fewer plaques accumulate outside the cell when tau is functioning.
Moussa has long sought a way to force neurons to clean up their garbage. In this study, he shows that nilotinib, a drug approved to treat cancer, can aid in that process. Nilotinib helps the neuron clear garbage, but requires some functional tau, he says. “This drug can work if there is a higher percentage of good to bad tau in the cell,” Moussa says. “There are many diseases of dementia that have malfunctioning tau and no plaque accumulation, such as frontal temporal dementia linked to Parkinsonism,” Moussa says. “The common culprit is tau, so a drug that helps tau do its job may help protect against progression of these diseases.”
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