MIT researchers have discovered a new method for reversing the effects of Alzheimer’s disease. The new finding demonstrates dramatic reductions in neurodegeneration.
The researchers used a peptide, which is an amino acid string. They were able to inhibit an enzyme that is typically overactive in the brains of those suffering from the disease.
The researchers discovered dramatic reductions in neurodegeneration and DNA damage in the brain after the chemical compounds blocked the hyperactive version of an enzyme called CDK5.
These tests were carried out on mice, and the results were significant and promising.
“This peptide has the ability to enter the brain”, said author Li-Huei Tsai, director of MIT’s Picower Institute for Learning and Memory.
“And in a couple of different models, the peptide shows protective effects against loss of neurons and also appears to be able to rescue some of the behavioral deficits”, he added.
The researchers hope that further testing will lead to the peptide being used as a treatment for patients with Alzheimer’s disease and other forms of dementia who have CDK5 overactivation.
According to MIT, the peptide does not interfere with CDK1, an essential enzyme that is structurally similar to CDK5, and it is similar in size to other peptide drugs used in clinical applications.
It went on to say, “CDK5 is activated by a smaller protein with which it interacts known as P35”.
“When P35 binds to CDK5, the structure of the enzyme changes, allowing it to phosphorylate (addition of a phosphate molecule to) its targets. P35, on the other hand, is cleaved into a smaller protein called P25 in Alzheimer’s and other neurodegenerative diseases, which can also bind to CDK5 but has a longer half-life than P35”, MIT added.
CDK5 becomes more active in cells when it binds to P25. CDK5 can also phosphorylate molecules other than its usual targets, such as the Tau protein, thanks to P25. Hyperphosphorylated Tau proteins form the neurofibrillary tangles that are a hallmark of Alzheimer’s disease.
Pharmaceutical companies have attempted to target P25 with small-molecule drugs, but because they also interfere with other cyclin-dependent kinases, none of them have been tested in patients.
When the peptide was tested in a mouse model of Alzheimer’s disease with hyperactive CDK5, the researchers observed a variety of beneficial effects, including reductions in DNA damage, neural inflammation, and neuron loss. These effects were much stronger in mouse studies than in cell culture tests.
In addition, the researchers reported that peptide therapy led to notable improvements in a separate mouse model of Alzheimer’s disease.
The researchers also examined the modifications in gene expression that take place in mouse neurons after exposure to the peptide.
The National Institutes of Health provided funding for the study.
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