Research Roundup: Alzheimer’s Memory Loss Reversed and More

Clinical research

Every week there are numerous scientific studies published. Here’s a look at some of the more interesting ones.

Alzheimer’s Memory Loss Reversed with Electromagnetic Waves

NeuroEM Therapeutics announced results from an open-label clinical trial that showed a reversal of cognitive impairment in Alzheimer’s disease after just two months of treatment. The results showed that the company’s wearable head device for in-home treatment, TEMT, was safe in the eight patients in the trial. The results are published in the Journal of Alzheimer’s Disease.

The patients were treated twice a day for one hour using NeuroEM’s first-in-class MemorEM head device. The head device uses multiple specialized emitters in the head cap that are activated sequentially. Evidence suggests that TEMT directly affects Alzheimer’s disease by penetrating the brain and brain cells to break up beta-amyloid and tau protein clusters. The company and its researchers are now planning a pivotal clinical trial of 150 mild to moderate Alzheimer’s patient later this year.

“We were particularly surprised that this highly significant improvement in the ADAS-cog was maintained even two weeks after treatment was completed,” said Gary Arendash, chief executive officer of NeuroEM Therapeutics. “The most likely explanation for continued benefit after cessation of treatment is that the Alzheimer’s disease process itself was being affected.”

Speeding the Drug Discovery Process

The biopharma industry is leveraging many different things to speed up the drug discovery process, ranging from high-throughput screening to artificial intelligence. Researchers with the Universite de Montreal (UdeM) and the Centre de Recherche de l’Hopital Ste-Justine developed a method of analysis using opioid analgesics as prototypes. It was possible to link simple cellular signals produced by opioids with the frequency of respiratory depression and other side effects were reported to the FDA.

“Thanks to your findings, we can now classify a large number of compounds while taking a multitude of cellular signals into account,” stated Michel Bouvier, the study’s co-senior author and principal investigator of molecular pharmacology and chief executive officer of UdeeM’s Institute for Research in Immunology and Cancer. “This wealth of comparisons this provides increases this classification’s predictive value for clinical responses. We think we can help patients by speeding up the drug discovery process so clinical trials can start earlier.”

Many new drugs fail in clinical trials because they don’t show sufficient therapeutic response. This test strategy infers possible clinical responses earlier in the drug discovery process, which could improve candidate selection. The research was published in the journal Nature Communications.

The authors wrote, “By classifying opioid ligands according to pathway-specific responses, it was possible to explore whether specific signals were driving typical side effects of opioids.”

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Eye Test for Alzheimer’s Disease?

Researchers believe that the rate at which a person’s eyes dilate during a cognitive test might be a low-cost method to screen for Alzheimer’s disease. A new study looked at pupillary responses driven by the locus coeruleus (LC), a group of neurons in the brainstem involved in regulating arousal and modulating cognitive function. LC drives pupillary response during cognitive tasks—the more difficult the task, the bigger the pupils dilate. The most recent study links pupillary dilation responses with risk genes associated with Alzheimer’s disease.

IDing a 3D Molecule Crucial to Cancer Development

Researchers at The Institute of Cancer Research, London, discovered the three-dimensional structure and function of a so-called “mix-n-match” protein that is involved in cancer progression and drug resistance. Th molecule is known as DHX8, which is part of a class of proteins involved in “alternative splicing,” which affects 95% of human genes. When alternative splicing malfunctions, it can cause changes to proteins that can lead to cancer or result in broader cancer diversity, evolution and drug resistance.

Drug to Treat Enlarged Prostate Potentially Slows Parkinson’s Progression

Collaborating researchers at the University of Iowa and Capital Medical University in Beijing, China, found that a drug used to treat enlarged prostate, terazosin, appears able to slow the progress of Parkinson’s disease. Terazosin, typically used to treat benign prostatic hyperplasia, or enlarged prostate, could also block cell death. This was related to the drug’s activation of an enzyme called PGK1, which is essential for the production of cellular energy. In analyzing several databases, they isolated 2,880 Parkinson’s patients taking one of the three drugs that target PGK1 and a comparison group of 15,409 Parkinson’s patients taking tamsulosin (Flonase). By tracking ICD-9/ICD-10 medical codes, they found that terazosin and similar drugs seem to decrease the symptoms and complications of Parkinson’s disease.

E. coli Toxin Linked to Cancer

Escherichia coli (E. coli), a human gut bacteria, is linked to colorectal cancer. New research has found out how an E. coli genotoxin called colibactin induces DNA double-strand breaks in eukaryotic cells, which increases the risk of colorectal cancer. They identified colibactin-645 and a metabolite pathway that directly linked colibactin to the increase in colorectal cancer.

Environmental Toxin Produced by Algae Linked to ALS

Using computer models, researchers linked an environmental toxin called beta-Methylamino-L-alanine (BMAA), produced by algal blooms in saltwater, to the development of amyotrophic lateral sclerosis (ALS). This has been, in particular, tied to high levels of BMAA in the Chamorro population of Guam where ALS is 100 times more common than other populations. BMAA is produced by cyanobacteria, a blue-green algae, and can accumulate in sharks, shellfish and bottom feeders. BMAA may integrate with a protein called copper-zinc superoxide dismutate (SOD1), which can adopt a form toxic to neurons.

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