Summary of MIT Neuroscientists Discover Way To Reverse Alzheimer’s Disease:
MIT neuroscientists have discovered a way to reverse neurodegeneration and other symptoms of Alzheimer’s by using a peptide inhibitor to block an overactive enzyme in patients’ brains called CDK5. CDK5 contributes to neurodegeneration in patients with Alzheimer’s and other neurodegenerative diseases. In experiments on mice, the researchers observed significant reductions in neurodegeneration, DNA damage, and improvements in cognitive abilities after treatment with the peptide inhibitor. The researchers hope that the peptide could eventually become a treatment for patients with Alzheimer’s and other forms of dementia.
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MIT Neuroscientists Develop Peptide Inhibitor to Reverse Alzheimer’s Symptoms
Researchers from the Massachusetts Institute of Technology (MIT) have found a way to reverse neurodegeneration in patients with Alzheimer’s disease and other forms of dementia. By blocking an overactive enzyme called CDK5, the team could observe significant reductions in neurodegeneration, DNA damage, and improved cognitive abilities. The peptide inhibitor used has the potential to treat Alzheimer’s and other forms of dementia caused by hyperactivation of CDK5 without interfering with essential enzymes. The study has been published in the Proceedings of the National Academy of Sciences.
CDK5’s Role in Disease
Li-Huei Tsai, the director of MIT’s Picower Institute for Learning and Memory, has been studying CDK5’s role in Alzheimer’s and other neurodegenerative diseases since early in her career. The enzyme is activated by another protein called P35 and plays a critical role in the central nervous system, regulating synaptic function.
In Alzheimer’s and other neurodegenerative diseases, P35 is cleaved into a minor protein called P25 with a longer half-life. This prolongs CDK5 activity, making it more active and contributing to the hyperphosphorylation of Tau protein. The increased activity of CDK5 and the accumulation of phosphorylated Tau proteins lead to neurofibrillary tangles, a hallmark of Alzheimer’s disease.
Design of Peptide Inhibitor
The MIT team designed a peptide inhibitor with a sequence identical to a critical structure, called the T loop, of CDK5. By having a similar system to the part of CDK5 that binds to P25, the peptide inhibitor prevents CDK5 from forming hyperactive complexes with P25.
Testing on Mice
Tests in lab-grown neurons showed modest reductions in CDK5 activity after treatment with the peptide inhibitor. The inhibitor did not affect other cyclin-dependent kinases or the standard CDK5-P35 complex.
Further testing on mice with Alzheimer’s disease showed reductions in DNA damage, neural inflammation, and neuron loss, along with improved cognitive abilities. The peptide also reduced Tau pathologies and neuron loss in mice with a mutant Tau protein.
Potential as a Treatment
The researchers hope their peptide inhibitor could eventually be used in clinical applications to treat patients with Alzheimer’s and other forms of dementia. The peptide is similar in size to other peptide drugs used clinically, and it does not interfere with CDK1, an essential enzyme structurally similar to CDK5.
Further Research
Tsai plans to study further the peptide inhibitor’s effects in mouse models of other diseases involving P25-associated neurodegeneration, such as frontotemporal dementia, HIV-induced dementia, and diabetes-linked cognitive impairment.
Conclusion
The MIT researchers’ peptide inhibitor shows potential as a treatment for Alzheimer’s and other forms of dementia caused by hyperactivation of CDK5. By blocking CDK5, the inhibitor reduces neurodegeneration and DNA damage and improves cognitive abilities. The inhibitor does not interfere with essential enzymes and could eventually be used as a treatment in clinical applications.
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