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Abstract

Alzheimer’s disease (AD) remains the most prevalent form of dementia, marked by progressive neurodegeneration and cognitive decline. This study synthesizes current knowledge of the molecular and cellular mechanisms driving AD and explores their translational potential into clinical interventions. Through an extensive secondary analysis of peer-reviewed literature, key pathogenic processes were identified, including amyloid-beta aggregation, tau hyperphosphorylation, neuroinflammation, and oxidative stress, each contributing to neuronal dysfunction and loss. Experimental models, such as transgenic mice and iPSC-derived neurons, consistently replicated these hallmarks, enabling identification of therapeutic targets like BACE1, GSK-3β, and the NLRP3 inflammasome. This is evident from the reviewed clinical trials where existing anti-amyloid drugs such as aducanumab and lecanemab reduces plaque in the brain but their impact on cognition remains limited.  While early diagnosis and staging have become possible by using biochemical markers like CSF amyloid-beta42, phospho-tau, and PET imaging there are several concerns such as its applicability in clinical practice.  It is clear that the pathology of AD is much more complicated than presumably represents simple mono-therapies and multi-target interference.  Therefore, the subsequent therapeutic approaches should involve system biology, combo drugs and personalized medications.  This work reframes the approach of addressing AD to a new level requiring large-scale therapeutic advances by simply bridging the gap between bench and clinic.