MIT scientists Thursday reported having potentially made a major breakthrough in the struggle against Alzheimer’s disease — one that produces “dramatic reductions” in neurodegeneration.
The hope centers on an unnamed peptide, or string of acids, that “interferes with,” or hampers the activity of, a particular enzyme known as CDK5. CDK5 is known to be overactive in the brains of Alzheimer’s patients and is believed to be behind a multitude of mechanisms by which cognitive decline and neurodegeneration occur.
Early tests conducted on mice revealed significant — and promising — results.
“We found that the effect of this peptide is just remarkable,” said study author Li-Huei Tsai, director of MIT’s Picower Institute for Learning and Memory. “We saw wonderful effects in terms of reducing neurodegeneration and neuroinflammatory responses, and even rescuing behavior deficits.”
“When the researchers tested the peptide in a mouse model of Alzheimer’s disease that has hyperactive CDK5, they saw a myriad of beneficial effects, including reductions in DNA damage, neural inflammation, and neuron loss,” the report said.
The peptide also was effective at mending the brain’s tau protein, which becomes a main characteristic of Alzheimer’s when altered.
The hope is, of course, as the New York Post reported, that this particular peptide might, with further testing, be developed into a treatment for dementia broadly.
The MIT report gave a glimpse of the variety of conditions that the breakthrough peptide shows the potential to treat, mentioning future plans to conduct a study to test the peptide’s effects on diabetes-linked cognitive impairment, for example. And Stuart Lipton, a neuroscience professor at Scripps Research, said the following:
“Further development of such peptide inhibitors toward a lead therapeutic candidate, if proven to be selective for the target and relatively free of clinical side effects, may eventually lead to novel treatments for neurodegenerative disorders ranging from Alzheimer’s disease to Frontotemporal dementia to Parkinson’s disease.”
The news tells part of the story about how the breakthrough came about. The “errant enzyme,” CDK5, becomes triggered into hyperactivity by a smaller protein called P35. This occurs when P35 is “cleaved,” producing a smaller protein known as P25, which also is connected to Parkinson’s disease. It is the P25 protein that affects the CDK5 enzyme.
Past efforts focused on targeting the P25 protein, but the treatments caused unacceptable levels of side effects, to the extent that they never reached the stage of being tested on patients. Li-Huei Tsai and her team approached the conundrum differently by utilizing the peptide to target CDK5 and its hyperactivity directly rather than targeting the P25 protein.
In addition to the breakthrough positive results, the peptide treatment did not interfere with normal CDK5 function and did not produce the side effects caused by efforts to target P25 proteins.
Future studies are expected to explore the peptide’s effect on frontotemporal dementia, HIV-induced dementia and diabetes-linked cognitive impairment.
“It’s very hard to say precisely which disease will most benefit, so I think a lot more work is needed,” Tsai said.
The research was funded by the National Institutes of Health.
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