United States: Presently, Alzheimer’s is set to be the most prevalent type of dementia, has been currently affecting 55 million people worldwide.
There are mainly two types of therapeutic approaches aimed at slowing or preventing the disease’s progression: one focuses on reduction of amyloid beta peptides, which form plaques in the area between brain cells, and another steering at the reduction of tau protein, which forms tangles toxic to neurons.
However, these strategies only distinguish a limited selection of biological markers and mechanisms that are associated with Alzheimer’s disease.
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Rick Hee, Jayesh Desai, Kristin Khandji, Nathan First, and Keiynne Barton have recently published the results of their clinical trial in Nature Medicine.
The clinical trial findings were conducted by a team of researchers from Western University, Stanford University, and University of California, San Francisco (UCSF), whose literature was published in Nature Medicine.
The team tried a new drug that has the potential to increase the ‘plasticity’ of brain to changes caused by Alzheimer, a breakthrough for mid-to-mod Alzheimer patient as this drug has received a first trial on human beings, as medicalxpress.com reported.
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The drug LM11A-31, invented by a Stanford professor, Dr. Frank Longo & UCSF professor, Dr. Stephen Mass is aimed at the P75 neurotrophin receptor (P75NTR) which is present on the cells in the brain.
P75NTR further assists in controlling different processes concerning cells’ live, growth and death, etc. such fulfill the role of the traffic light controller that let some signals pass and other do not. It acted to amplify the signals that were pro-survival and the growth of cells.
The developers of the drug 2020 approached Taylor Schmitz, who is a professor at Schulich School of Medicine & Dentistry professor Taylor Schmitz and Hayley Shanks, a neuroscience Ph.D. student at Schulich Medicine & Dentistry, to help in analyzing the structural MRI data of their phase 2A clinical trial.
They primarily expanded their studies to include positron emission tomography (PET) with cerebrospinal fluid results.
Indeed, while the trial’s design aimed at assessing the safety and the tolerability of the drug in patients with mild to moderate Alzheimer’s, investigators also collected several indicators of brain disease state to ascertain whether the drug was also able to influence the progression of the disease between baseline and follow-up assessment in comparison with placebo.
According to the targets set, the trial fulfilled the primary objectives, demonstrating the safety and tolerability of the investigational product.
The participants in the trial were examined by the team at Western in the directions of the main analysis. They showed that the drug blunt the disease progression as compared with the control group throughout the study despite the study duration being only 26 weeks.
“In a phase 2A clinical trial, the goal for the medication is to ascertain that it is not inducing toxicity effects,” said Schmitz, lead author.
The researchers would like to observe that the given drug can be helpful for the patients even in case of its use later on in the development of the disease.
Even drugs that aim at removing amyloid from the brain, like amyloid monoclonal antibodies, to treat patients at different stages of the disease will be less effective for those suffering from Alzheimer’s disease as the amyloid has already affected the neurons and the brain.
Shanks added, “The reason this drug is exciting is because it’s directly affecting the ability of the neurons to survive. It promotes their overall integrity, their branching and their synapses [where they connect and communicate with each other],” as medicalxpress.com reported.