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Alzheimer's Disease Research and Treatments / Dementia and Cognitive Impairment Research / Clusterin in Disease Pathology · Journal article
Middle East Research Journal of Medical Sciences · August 5, 2026
A consensus or society position rather than new primary data.
This is a narrative review summarizing the genetic basis of Alzheimer's disease, including causal genes (APP, PSEN1, PSEN2, BACE1) and susceptibility loci identified by GWAS, molecular pathways, and current and emerging therapeutic approaches. It does not present new empirical evidence or clinical trial results, but rather synthesises existing knowledge for an overview of the field.
Journal article. Individuals with Alzheimer's disease worldwide; review does not focus on a specific enrolled cohort..
Alzheimer's disease accounts for approximately 60–70% of all dementia cases worldwide Over 55 million individuals currently affected; projected to reach 139 million by 2050 Early-onset familial AD associated with mutations in APP, PSEN1, PSEN2, and BACE1
Therapeutic efficacy and safety data for mentioned interventions not detailed or critically evaluated.
This review provides clinicians and researchers with a comprehensive synthesis of known genetic risk factors and molecular pathways in AD, and discusses current and emerging therapeutic strategies. However, as a narrative review without new empirical data, it should be used to inform understanding of the field rather than as evidence for specific clinical interventions.
This is a comprehensive narrative review synthesizing current knowledge of AD genetics, pathways, and therapeutic targets rather than presenting original research evidence or clinical trial data.
As stated by the source record.
Quoted from the source exactly as published.
This review provides clinicians and researchers with a comprehensive synthesis of known genetic risk factors and molecular pathways in AD, and discusses current and emerging therapeutic strategies. However, as a narrative review without new empirical data, it should be used to inform understanding of the field rather than as evidence for specific clinical interventions.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Alzheimer's disease (AD) is the leading cause of dementia worldwide, accounting for approximately 60–70% of all dementia cases. It is a progressive neurodegenerative disorder that results in memory loss, cognitive decline and functional impairment, and affects over 55 million individuals worldwide. The number of affected individuals is projected to reach 139 million by 2050, posing a substantial public health and socioeconomic burden. Pathologically, AD is defined by extracellular deposits of amyloid-β (Aβ) plaques and intracellular accumulation of hyperphosphorylated tau in the form of neurofibrillary tangles (NFTs). There is growing evidence that the pathogenesis of AD is multifactorial, involving genetic, molecular, and environmental factors. This review aims to give a comprehensive overview of the major genes and molecular pathways involved in the pathogenesis of AD, as well as recent advances in genome-wide association studies (GWAS) and emerging therapeutic strategies. The mutations in amyloid precursor protein (APP), presenilin 1 (PSEN1), presenilin 2 (PSEN2), and β-site amyloid precursor protein cleaving enzyme 1 (BACE1) are associated with early-onset familial AD, while late-onset AD is linked to several susceptibility genes identified by GWAS. The molecular mechanisms underlying AD pathogenesis and progression are discussed with respect to major AD-associated genes, such as microtubule-associated protein tau (MAPT), apolipoprotein E (APOE), triggering receptor expressed on myeloid cells 2 (TREM2), sortilin-related receptor 1 (SORL1), bridging integrator 1 (BIN1), phosphatidylinositol-binding clathrin assembly protein (PICALM), Clusterin (CLU), ATP-binding cassette subfamily A member 7 (ABCA7), complement receptor 1 (CR1), acetylcholinesterase (AChE), nuclear factor erythroid 2-related factor 2 (NRF2), and tumor necrosis factor (TNF). Current therapeutic strategies, including anti-amyloid immunotherapy, AChE inhibitors, tau-directed therapies, and emerging gene-targeted approaches, are also discussed. In addition, progress in multi-omics technologies, disease models using induced pluripotent stem cells (iPSC), gene editing with CRISPR-Cas9, and artificial intelligence (AI) analysis are likely to speed up the implementation of precision medicine for early diagnosis, risk prediction, and treatment of Alzheimer's disease.
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