ASU researchers propose a unifying explanation for molecular chaos driving Alzheimer’s disease

In a groundbreaking theory, scientists from the Bodesign Institute of Arizona State University propose an unknown explanation for the molecular chaos that drives Alzheimer’s disease. The condition causes widespread disruption of gene behavior, which influences every known neuropathology and clinical manifestation of the disease.

According to the analysis, the changes caused by the disease may arise from a breakdown in the transport system that vital molecules between the cell nucleus and cytoplasm, the liquid environment around the core around the core where many essential processes occur. The scale of disruption, involving more than 1,000 genes, underlines the complexity of Alzheimer’s.

The sabotage of cellular messages, activated by the formation of chronic pellets in the brain, can be a key factor in the development of Alzheimer’s and other neurodegenerative diseases – just like a city -wide power outages that shut off critical systems. Stress pellets are lumps of proteins and RNA that form in response to cell stress.

The assessment, led by Paul Coleman and colleagues with the ASU banner Neurodegenerative Disease Research Center, emphasizes that gene expression – the process with which genes produce the proteins that are essential for the cell function – is changed on a huge scale in Alzheimer’s.

These changes influence the correct functioning of synapses in the brain, as well as metabolism, protein processing and cell survival. The research could show the road to radically new approaches to tackle Alzheimer’s disease in the earliest stages.

Our proposal, aimed at the breakdown of communication between the core and the cytoplasm that leads to massive disruptions in gene expression, offers a plausible framework to fully understand the mechanisms that control this complex disease. Studying these early manifestations of Alzheimer’s could paved the way for innovative approaches to diagnosis, treatment and prevention, in which the disease is tackled on its roots. “

Paul Coleman, ASU-Banner Neurodegenerative Disease Research Center

Coleman is accompanied by Elaine Delvaux, Ashley Boehringer, Carol Huseby and center director Jeffrey Kordower.

The research results appear in the current number of Alzheimer & Dementia: The Journal of the Alzheimer’s Association.

The confused web of a disease

Alzheimer’s disease remains one of the most devastating and mysterious disorders of the medical sciences, which often seem like many diseases are rolled into one. The symptoms range from memory loss and cognitive decline to personality changes, all driven by complex biological disturbances.

This makes it incredibly difficult for researchers to determine a single cause or to develop effective treatments, which means that millions of families struggle with its devastating effects.

Despite more than a century of intense research and billions invested dollars, there is still no treatment to stop or cure the disease. In the meantime, the global costs of dementia -care remain amazingly high. In 2019, the worldwide costs of dementia were estimated at $ 1.3 trillion, a figure that would be expected to rise to $ 2.8 trillion in 2030, according to Alzheimer Disease International.

Earlier research has focused on tangible symptoms of the disease, such as amyloid plaques, tau tangs, inflammation and cellular dysfunction, but no explanation has arisen to unite these phenomena.

The research suggests that these changes can be traced to a disruption in the transport system of the cell, which moves crucial molecules such as RNA and proteins between the core and the surrounding cytoplasm. This failure disrupts the production of essential proteins and changes the chemical switches that regulate gene activity.

The role of stress pellets

The research highlights chronic stress pellets such as the primary culprits in this process. Stress pellets are structures that temporarily form in response to cell stress, which means that non -essential processes are paused while the cell is recovering. Normally they protect the cell during stressful conditions and dissolve as soon as the stress decreases.

In Alzheimer’s disease, however, these grains remain abnormal existence and become chronic and pathological, catching vital molecules and hinder their movements in and out of the cell nucleus. Instead of offering protection, they cause damage and contribute to the progression of the disease.

Different genetic and environmental factors – including certain genes, inflammation, exposure to pesticides, viruses and air pollution – can contribute to cellular stress.

This stress response and grain formation can then cause a cascade, leading to disruption of the nucleus-to-care-inoplasma transit system. It is like a clogged highway that prevents the movement of critical goods, so that resources remain and cause chaos on both sides of the communication hub.

In particular, it is assumed that these radical changes take place at a very early stage of the disease, long before the appearance of clinical symptoms. One of the most striking of these later manifestations are amyloid plaques, which are lumps of incorrectly folded proteins that disturb between neurons and disrupt cell communication, and tau tangs – twisted fibers of a protein that builds up in neurons, who affect their function and affect their function and Ultimately lead to cell death.

The prospect of early interventions aimed at stress pellets offers a potentially transforming approach to combating Alzheimer’s disease. By identifying and tackling the formation of pathological stress pellets in the earliest stages, it may be possible to stop the beginning of symptoms such as amyloid plaques and tau tangs and the devastating cognitive consequences of the disease or to slightly delay.

“Our paper contributes to the current debate when Alzheimer’s really starts – an evolving concept formed by progress in technology and research,” says Coleman.

“The most important questions are when it can be detected for the first time and when intervention should begin, both of which have in -depth implications for society and future medical approaches.”

Such an approach could shift the focus of the treatment of Alzheimer’s in order to manage the symptoms of later stage to prevent the disease from making full progress. Although these interventions are still in the research phase, they emphasize a promising path for understanding and reducing the underlying mechanisms of the disease.