Newly Discovered Brain Plaque in Alzheimer’s Disease

Scientists have unveiled a novel brain plaque type that may reshape the understanding of Alzheimer’s disease, pointing to fresh avenues for treatment. Researchers at the University of Minnesota have named these structures “mitochondrial plaques.” These plaques have been identified in both preclinical models and human brain tissue and have been reported in Nature Neuroscience.

The findings suggest that mitochondrial plaques could appear earlier than the well-researched beta-amyloid plaques, which are traditionally seen as a hallmark of Alzheimer’s. Alzheimer’s disease is known for the gradual loss of brain cells, leading to cognitive decline. Historically, research has focused on beta-amyloid plaques and neurofibrillary tangles that accumulate in the brain as the disease worsens.

The newly recognized plaques appear to form independently of traditional amyloid plaques. They may manifest in the early stages of the disease. The study noted that mitochondrial plaques contain high levels of amyloid precursor protein, which leads to beta-amyloid formation. As Alzheimer’s progresses, mitochondrial plaques often appear alongside traditional amyloid plaques. Researchers suggest this could contribute to the development of the disease’s characteristic brain changes.

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

Unlike traditional amyloid plaques that form outside brain cells, the newly discovered plaques appear to impact neurons directly. This distinction makes them a potential target for new Alzheimer’s treatments. According to Xiuli Dan, a research assistant professor and the study’s first author, understanding these formations might lead to new strategies to slow or even prevent the disease.

The discovery suggests Alzheimer’s-related changes might start earlier and via different biological pathways than formerly assumed. However, experts urge caution. More research is required to fully comprehend the finding’s significance. Laura Bojarskaite, a neuroscientist at the University of Oslo, emphasized the need for further investigation. She indicated that if these findings are substantiated, they could alter how Alzheimer’s onset is understood.

For years, research has centered on extracellular amyloid plaques. The new discovery shifts focus to processes within neurons. Bojarskaite notes that identifying an early biological change doesn’t guarantee it causes the disease. She questions whether mitochondrial plaques actively contribute to neurodegeneration or if they reflect preexisting stress in neurons.

The study probes a longstanding question in Alzheimer’s research: the role of mitochondrial dysfunction. While atypical mitochondrial function is evident in Alzheimer’s, whether it causes the disease or results from other changes remains unclear. The discovery may hold practical implications if confirmed. Mitochondrial plaques might serve as early disease markers, aiding in early intervention. Additionally, therapies might evolve to conserve mitochondrial function rather than focusing only on amyloid.

Bojarskaite urges caution, calling for independent replication of the results and observation in living patients. She emphasizes that understanding these findings is a promising step rather than a definitive change in practice.

Researchers at the University of Minnesota aim to identify biomarkers linked to mitochondrial plaques and screen for drugs to prevent their accumulation. They hope this will reveal whether these new structures play a direct role in Alzheimer’s disease and whether targeting them can slow disease progression.