Newswise — Philadelphia—Researchers at the Alzheimer’s Center at Temple University (ACT) have published a comprehensive new review examining how two hallmark proteins of Alzheimer’s disease, amyloid-β and tau, interact and reinforce one another to drive disease progression. Under the guidance of Domenico Praticò, MD, Professor of Neurosciences, the paper investigates the latest data on the behavior of the plaques and tangles responsible for dementia.
Causing cognitive impairment and memory loss, Alzheimer’s disease is marked by the accumulation of amyloid-β plaques and tau tangles in the brain. While both pathologies have long been studied independently, growing evidence suggests that their interaction plays a central role in triggering synaptic dysfunction, neurodegeneration, and the progressive cognitive decline seen in patients.
“This review brings together recent advances showing that amyloid-β and tau are not acting in isolation,” said Praticò, who is also the Scott Richards North Star Charitable Foundation Chair in Alzheimer’s Research at the Lewis Katz School of Medicine at Temple University. “Instead, they engage in a complex and synergistic relationship that accelerates disease onset and progression.”
The paper demonstrates that synaptic dysfunction occurs early in Alzheimer’s disease, preceding widespread neuronal loss. As the disease advances, this dysfunction gives way to neurodegeneration and irreversible neuronal cell death.
“The molecular mechanisms through which amyloid-β can promote tau pathology, and vice versa,” said Praticò, “amplifies damage within vulnerable brain circuits.”
By critically evaluating recent findings, the paper provides a framework for understanding how these pathological processes intersect across different stages of the disease. The authors found that interplay between amyloid-β and tau may inform the development of more effective therapeutic strategies aimed at slowing or preventing disease progression.
“Our goal was to offer a unified perspective that can help guide future research,” Praticò said. “A clearer understanding of how these two proteins interact may open new directions for treatment approaches that target Alzheimer’s disease earlier and more precisely.”
The review, titled “Amyloid-β and Tau in Alzheimer’s Disease: Pathogenesis, Mechanisms, and Interplay,” was published online January 9, 2026 in the journal Cell Death & Disease.
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