Scientists have discovered a new form of brain plaque, termed “mitochondrial plaques,” that could transform current understanding of Alzheimer’s disease. Researchers at the University of Minnesota uncovered this feature in both preclinical disease models and human brain tissue. Their findings, shared in Nature Neuroscience, highlight that these plaques might appear before the widely studied beta-amyloid plaques.
Alzheimer’s is marked by the slow degradation of brain cells and cognitive abilities. Historically, research has concentrated on beta-amyloid plaques and neurofibrillary tangles. Now, mitochondrial plaques appear to be forming independently of these known plaque types and potentially emerge in the condition’s earliest stages.
The study notes that mitochondrial plaques are rich in amyloid precursor protein, which generates beta-amyloid. As Alzheimer’s progresses, these plaques are often found with traditional ones, suggesting they may contribute to familiar brain changes associated with the disease.
“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. “By understanding how these plaques form and contribute to disease progression, we may develop new strategies to slow or even prevent Alzheimer’s disease.”
These mitochondrial plaques differ from traditional amyloid plaques as they affect neurons directly, making them a potential target for future Alzheimer’s treatments, according to Xiuli Dan, lead author of the study.
The discovery indicates Alzheimer’s-related changes might begin through unknown pathways, earlier than expected. Yet, experts call for further research to understand this finding fully. If confirmed, these findings could revolutionize the perception of Alzheimer’s onset, as expressed by Laura Bojarskaite, a neuroscientist from the University of Oslo. However, Bojarskaite emphasizes that early biological shifts do not automatically equate to causation of the disease.
The study also explores mitochondrial dysfunction’s role in Alzheimer’s. While it is known that mitochondria malfunction in Alzheimer’s, the precise connection between these problems and the disease remains unclear. Scientists are trying to determine if mitochondrial changes are widespread across patients or represent one of many paths within this complex disease.
If subsequent research confirms that mitochondrial plaques form first, their presence might act as early indicators for Alzheimer’s, aiding in identifying at-risk individuals sooner. Such advancements could lead to therapies focused on preserving mitochondrial function instead of just targeting amyloid.
Bojarskaite advises cautious optimism around these findings, as much work remains. Upcoming efforts by the University of Minnesota include identifying biomarkers associated with mitochondrial plaques and screening potential drugs to prevent their accumulation. This research will shed light on whether these newfound structures directly impact Alzheimer’s and whether they can be targeted to slow its progression.