Could a new approach stop or slow the progression?

For this study, the researchers focused on a protein called plexin-B1.

“Plexin-B1 is a membrane receptor, originally identified as an axon guidance molecule important for axon wiring during neurodevelopment,” the study authors explained. MNT.

“A recent big data analysis by Dr. Bin Zhang’s systems biology group computationally identified plexin-B1 as a central gene driving late-onset Alzheimer’s disease,” they told us.

“This project presents a team approach from three different laboratories – therefore three lead authors – to address the function of plexin-B1 in Alzheimer’s disease for the first time,” the study authors noted.

Scientists examined how the plexin-B1 protein interacts with reagents astrocytes — cells of the central nervous system, including the brain, that activate in response to illness or injury.

The lead authors explained that:

“Astrocytes are a type of glial cell that supports neuronal function. Reactive astrocytes respond to Alzheimer’s disease by surrounding amyloid plaques, forming a structure called (a) glial net.”

“Our study found that plexin-B1 activation in reactive astrocytes prevents them from (functioning properly) to clear plaques,” they continued. “Removal of plexin-B1 may reverse this situation, leading to better amyloid clearance and less plaque burden.”

The three researchers are currently working to find therapeutic ways to target plexin-B1. Zhang’s team is apparently attempting to identify drug candidates using artificial intelligence Approaches assisted by (AI). And Zou and Friedel’s labs are teaming up to generate function-blocking antibodies against plexin-B1.

“The three teams will work together to identify drugs or antibodies effective in modulating plexin-B1 function in reactive astrocytes,” the study authors said. “We believe our research will contribute significantly to the global effort to combat Alzheimer’s disease.”

“This study not only confirms one of the most important predictions of our genetic network models, but it also significantly advances our understanding of Alzheimer’s disease. This lays a solid foundation for developing new therapies targeting such highly predictive network models,” they argued.

“Our study opens new avenues for Alzheimer’s disease research, highlighting the importance of cellular interactions in the development of treatments against neurodegenerative diseases.”

–Roland H. Friedel, PhD; Hongyan Zou, MD, PhD; Bin Zhang, Ph.D.

After reviewing this study, Karen D. Sullivan, PhD, ABPP, board-certified neuropsychologist, owner of I CARE FOR YOUR BRAIN and Reid Healthcare Transformation Fellow at FirstHealth of the Carolinas in Pinehurst, North Carolina, who was not involved in the research. , said MNT this innovative study offers a new window of hope for the treatment of Alzheimer’s disease.

“With so many treatments focused on beta-amyloid, this evidence suggests that by relaxing the spacing of “connector cells,” i.e., glial, we may be able to reduce neuroinflammation and help Alzheimer’s disease plaques be more compact,” Sullivan continued. “In turn, this should reduce the number of neurons consumed by the disease, i.e. less cell death.”

However, the research is still at an early, preclinical stage, she cautioned.

“This study was performed in a genetic mouse model of Alzheimer’s disease,” Sullivan noted. “We always want to see results like this translate well to the human brain before we get too hopeful that a new drug can be developed from this discovery.”

MNT also spoke with Clifford Segil, DO, a neurologist at Providence Saint John’s Health Center in Santa Monica, California, about this study. Segil was also not involved in this research.

Segil expressed further doubts about the therapeutic potential linked to the results of this study. Targeting plaque buildup in the brain isn’t necessarily the best way to fight Alzheimer’s, he says.

Without mincing words, he said: “It irks me to see researchers blindly observing that cognitive decline and memory loss due to neurodegeneration are linked to beta-amyloid and neurofibrillary tangles, while clinicians on the front lines treating and diagnosing patients with dementia continues to deteriorate. “the amyloid hypothesis”, because clinically available and highly effective anti-amyloid drugs continue to produce modest improvements in cognition according to data provided by the pharmaceutical company and without any notable clinical improvement to (a) clinical neurologist.

Referring to the recent controversy that casts a shadow of doubt on the widely held hypothesis that beta-amyloid plaques are at least partly present in the brain for the symptoms of Alzheimer’s disease, Segil pointed out that :

“This article’s claim that amyloid and tangles cause cognitive decline and memory loss becomes less and less credible over time as anti-brain amyloid drugs are used and patients receiving these drugs in the real world do not show any significant improvement.”

He also noted that many clinicians like him see patients with high brain amyloid burden without any cognitive problems, as well as those with low brain amyloid burden and disabling and severe cognitive impairment.

“Findings focused on eliminating amyloid plaque buildup will not help find new ways to treat memory loss in patients with Alzheimer’s dementia,” Segil asserted.

Nevertheless, he welcomed some of the results from other studies with more enthusiasm, saying: “I am eager to see whether the plexin-B1 noted in this study which acts on the cells supporting brain neurons or on the Glial cells may produce memory enhancements distinct from their effects on brain amyloid.

“I would like to see more research done on brain microglia and (the) lymphatic system of the brain“added Segil. “When I received my BSc in Neuroscience in 1996, there was no agreement at the time that the brain had a lymphatic system, and further research should be done into new ways to activate the functioning of microglial cells in the brain regarding memory loss,” he told us.