ABS 045: The Curious Case of Tau: Exploring the Role of Tau Protein in Alzheimer’s Disease

Chelsea Ohanaga ¹, Mayon Machaiah Merianda ², Rafael Rodriguez ³, Pearl Lin ⁴, Sajiri Wani ⁵, Lauren Gonzalez-Perez ⁶, Hazel Tran ⁷, Alisha Singh ⁸; 2. Independence High School 3. New York University 4. Bel Air High School 5. North Penn High School 6. Math and Science College Preparatory 7. University of California, Davis 8. Parkway West High School

¹ University of California, Los Angeles
² Independence High School
³ New York University
⁴ Bel Air High School
⁵ North Penn High School
⁶ Math and Science College Preparatory
⁷ University of California, Davis
⁸ Parkway West High School

The Van Wickle Journal (2026) Volume 2, ABS045

Introduction: Alzheimer’s disease (AD) is a neurodegenerative disorder marked by progressive memory loss and cognitive decline. Prior research has shown that abnormal tau protein forms neurofibrillary tangles that destabilize microtubules and interfere with synaptic signaling which weakens the neuronal communication needed for learning and memory. Studies also suggest that pathological tau disrupts calcium homeostasis, a process essential for synaptic plasticity and neuronal survival. However, the specific mechanisms linking tau-induced calcium imbalance to deficits in synaptic signaling and memory remain unclear. There has been little evidence to fill in the gap between disruptions in calcium homeostasis caused by pathological tau and the downstream mechanisms that produce cognitive deficits. This gap is significant because calcium regulation is central to how neurons adapt and store information. Understanding this missing link may reveal new therapeutic targets. This study aims to address that gap by examining how tau-related disruptions in calcium homeostasis contribute to synaptic dysfunction and, ultimately, memory decline in individuals with AD.

Methods: We performed a bibliometric literature review to identify the top-100 most-cited articles in AD research. We began by systematically searching scientific databases, including Web of Science (WoS), PubMed, and Scopus, for neurodegenerative disease studies and compiling a preliminary list based on citation metrics and relevance. Articles meeting our criteria were analyzed using bibliometric software (R’s bibliometrix package, R Studio) to map author networks, visualize publication patterns, and quantify research impact. The WoS platform enabled detailed filtering and export of citation data, supporting robust analyses of co-authorship, journal distribution, and research trends. Visualizations were generated to highlight dominant journals and collaboration networks among lead and senior authors. We then conducted literature reviews of selected key papers from the top-100 list, summarizing foundational advances in mechanisms, diagnostics, and therapeutic strategies in AD. This approach ensured comprehensive coverage of the most influential research and captured evolving trends in neurodegenerative disease scholarship.

Results: Our findings revealed that highly cited work is concentrated among a small number of senior authors and top research institutions, emphasizing the importance of collaboration networks and well-funded research environments in driving impactful discoveries. Across these important studies, we found that abnormal tau and beta amyloid interactions could disrupt calcium homeostasis, synaptic signaling, and ultimately, the neural circuits responsible for memory. The literature strongly pushes forward the idea that soluble beta amyloid oligomers initiate downstream tau pathology, which contributes to inflammation, structural instability, and impaired synaptic plasticity.

Discussion: These results highlight a converging mechanism in which tau mediated calcium imbalance serves as a link between molecular pathology and cognitive decline. On a broader scale, our study underscores how research priorities, which are shaped by influential authors, journals, and institutions, guide the scientific community’s understanding of AD mechanisms and potential treatments. For future research, experimental studies should directly test how tau driven calcium imbalance alters specific synaptic pathways, especially those involved in long term potentiation and memory encoding. Future work should also include refining early diagnostic markers that track both beta amyloid and tau pathology simultaneously, improving early detection.