A team of researchers led by Professor Yan-Jiang Wang has published a review arguing that Alzheimer's disease requires integrated treatments targeting multiple factors, not single causes. New drugs like lecanemab and donanemab offer modest benefits by slowing decline, but fall short of reversal. The paper, in Science China Life Sciences, emphasizes genetics, aging, and systemic health alongside amyloid-beta and tau proteins.
Alzheimer's disease erodes memory and thinking, posing a growing challenge with aging populations. Professor Yan-Jiang Wang and colleagues, including Yu-Juan Jia and Jin-Tai Yu, detailed in their review why past efforts focusing on one factor, such as amyloid-beta buildup, have yielded limited success. They highlight the interplay of amyloid-beta, tau protein tangles via hyperphosphorylation, genetic risks like APOE ε4, aging processes, and conditions including insulin resistance and hypertension. Gut-brain connections also influence progression, the authors note. New monoclonal antibodies lecanemab and donanemab slow cognitive decline modestly. Yet, the researchers stress that these do not restore brain function, underscoring the need for broader approaches. Advances like CRISPR/Cas9 gene editing target genetic risks, while senolytic therapies aim to clear aging glial cells. Existing diabetes drugs and gut health interventions show promise for systemic effects. The team advocates shifting from reductionist methods to integrated strategies, using tools like human iPSC-derived organoids for testing and biomarkers such as plasma pTau217 for early detection. Precision medicine could enable tailored, early interventions. 'Success in defeating Alzheimer's hinges on interdisciplinary collaboration and holistic innovation,' the authors conclude, outlining a path to manage or prevent the condition.