Scientists have identified a previously unknown type of brain plaque that could reshape understanding of how Alzheimer's disease develops and potentially open the door to new treatment strategies.

Researchers at the University of Minnesota reported the discovery of what they call "mitochondrial plaques," a newly recognized feature of Alzheimer's disease found in both preclinical disease models and human brain tissue. The findings, published in Nature Neuroscience, suggest these plaques may appear earlier than the better-known beta-amyloid plaques that have long been considered a hallmark of the disease.

Alzheimer's disease is characterized by the gradual loss of brain cells and cognitive function. For decades, much of the research focus has been on beta-amyloid plaques and neurofibrillary tangles, which accumulate in the brain as the disease progresses. The newly identified mitochondrial plaques appear to form independently of traditional amyloid plaques and may emerge at the earliest stages of the condition.

The study found that mitochondrial plaques contain high levels of amyloid precursor protein, the molecule that gives rise to beta-amyloid. As Alzheimer's advances, mitochondrial plaques are frequently found alongside traditional amyloid plaques, leading researchers to suggest they may contribute to the development of the disease's classic brain changes.

"This discovery identifies mitochondrial plaques as a previously unrecognized feature of Alzheimer's disease," Paul Robbins, a professor at the University of Minnesota Medical School and associate director of the Masonic Institute on the Biology of Aging and Metabolism, said in a statement.

"By understanding how these plaques form and contribute to disease progression, we may be able to develop new strategies to slow or even prevent Alzheimer's disease."

Unlike traditional amyloid plaques, which are found outside brain cells, the newly identified plaques appear to directly affect neurons, which makes them a potential new target for Alzheimer's disease treatments, according to Xiuli Dan, a research assistant professor and first author of the study.

The findings raise the possibility that Alzheimer's-related changes could begin earlier and through different biological pathways than previously thought. However, experts caution that more research will be needed before the discovery's significance is fully understood.

Laura Bojarskaite, a neuroscientist at the University of Oslo who was not involved in the research, said that if the findings are confirmed, they could alter scientists' understanding of how Alzheimer's begins.

"If these findings hold up, they could be quite important because they suggest that Alzheimer's pathology may begin earlier—and through different biological processes—than we previously recognized," she told Newsweek.

For decades, researchers have largely concentrated on extracellular amyloid plaques. Bojarskaite said the discovery could shift attention toward processes occurring inside neurons before the disease's traditional hallmarks become visible.

At the same time, she emphasized that an early biological change is not necessarily the cause of the disease.

"The key question is whether these mitochondrial plaques actively contribute to neurodegeneration or simply reflect neurons already under stress," she said.

The study also touches on a long-standing question in Alzheimer's research: the role of mitochondrial dysfunction. While scientists know mitochondria often function abnormally in Alzheimer's disease, Bojarskaite said it remains unclear whether these problems help trigger the disease or emerge as a consequence of other changes already underway.

She added that researchers still need to understand why some neurons appear particularly vulnerable and whether mitochondrial alterations are common across most patients or represent only one pathway within a complex and biologically diverse disease.

The discovery could eventually have practical implications if future research confirms that mitochondrial plaques form before traditional amyloid plaques. In that scenario, they might serve as biomarkers for identifying people at risk earlier in the disease process, when interventions may be more effective. The findings could also inspire therapies designed to preserve mitochondrial function rather than focusing exclusively on amyloid.

However, Bojarskaite stressed that several hurdles remain. The results will need to be independently replicated, observed in living patients and shown to predict disease progression before they can be translated into clinical applications.

For now, she urged caution when interpreting the findings.

"People should see studies like this as promising, not practice-changing," Bojarskaite said.

The University of Minnesota team's next steps include identifying biomarkers linked to mitochondrial plaques and screening for drugs that could prevent them from accumulating, work that researchers hope will clarify whether the newly discovered structures play a direct role in Alzheimer's disease and whether they can ultimately be targeted to slow its progression.

Reference:

Xiuli Dan et al, Mitochondrial accumulation and lysosomal dysfunction result in mitochondrial plaques in Alzheimer's disease, Nature Neuroscience (2026). DOI: 10.1038/s41593-026-02390-1

Contact Newsweek editors on this story: Kara Dolman and Emma Lee-Sang