Ageing Research Reviews最新文献

{"title":"Unraveling the protein post-translational modification landscape: Neuroinflammation and neuronal death after stroke","authors":"Jin Tao ,&nbsp;Jiaxin Li ,&nbsp;Xiaochong Fan ,&nbsp;Chao Jiang ,&nbsp;Yebin Wang ,&nbsp;Mengzhe Qin ,&nbsp;Zahra Nikfard ,&nbsp;Fatemeh Nikfard ,&nbsp;Yunchao Wang ,&nbsp;Ting Zhao ,&nbsp;Na Xing ,&nbsp;Marietta Zille ,&nbsp;Junmin Wang ,&nbsp;Jiewen Zhang ,&nbsp;Xuemei Chen ,&nbsp;Jian Wang","doi":"10.1016/j.arr.2024.102489","DOIUrl":"10.1016/j.arr.2024.102489","url":null,"abstract":"<div><p>The impact of stroke on global health is profound, with both high mortality and morbidity rates. This condition can result from cerebral ischemia, intracerebral hemorrhage (ICH), and subarachnoid hemorrhage (SAH). The pathophysiology of stroke involves secondary damage and irreversible loss of neuronal function. Post-translational modifications (PTMs) have been recognized as crucial regulatory mechanisms in ischemic and hemorrhagic stroke-induced brain injury. These PTMs include phosphorylation, glycosylation, ubiquitination, SUMOylation, acetylation, and succinylation. This comprehensive review delves into recent research on the PTMs landscape associated with neuroinflammation and neuronal death specific to cerebral ischemia, ICH, and SAH. This review aims to explain the role of PTMs in regulating pathologic mechanisms and present critical techniques and proteomic strategies for identifying PTMs. This knowledge helps us comprehend the underlying mechanisms of stroke injury and repair processes, leading to the development of innovative treatment strategies. Importantly, this review underscores the significance of exploring PTMs to understand the pathophysiology of stroke.</p></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"101 ","pages":"Article 102489"},"PeriodicalIF":12.5,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142238630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"On the interface of aging, cancer, and neurodegeneration with SIRT6 and L1 retrotransposon protein interaction network","authors":"Jarmila Nahálková","doi":"10.1016/j.arr.2024.102496","DOIUrl":"10.1016/j.arr.2024.102496","url":null,"abstract":"<div><div>Roles of the sirtuins in aging and longevity appear related to their evolutionarily conserved functions as retroviral-restriction factors. Retrotransposons also promote the aging process, which can be reversed by the inhibition of their activity. SIRT6 can functionally limit the mutation activity of LINE-1 (L1), a retrotransposon causing cancerogenesis-linked mutations accumulating during aging. Here, an overview of the molecular mechanisms of the controlling effects was created by the pathway enrichment and gene function prediction analysis of a protein interaction network of SIRT6 and L1 retrotransposon proteins L1 ORF1p, and L1 ORF2p. The L1-SIRT6 interaction network is enriched in pathways and nodes associated with RNA quality control, DNA damage response, tumor-related and retrotransposon activity-suppressing functions. The analysis also highlighted sumoylation, which controls protein-protein interactions, subcellular localization, and other post-translational modifications; DNA IR Damage and Cellular Response via ATR, and Hallmark Myc Targets V1, which scores are a measure of tumor aggressiveness. The protein node prioritization analysis emphasized the functions of tumor suppressors p53, PARP1, BRCA1, and BRCA2 having L1 retrotransposon limiting activity; tumor promoters EIF4A3, HNRNPA1, HNRNPH1, DDX5; and antiviral innate immunity regulators DDX39A and DDX23. The outline of the regulatory mechanisms involved in L1 retrotransposition with a focus on the prioritized nodes is here demonstrated in detail. Furthermore, a model establishing functional links between HIV infection, L1 retrotransposition, SIRT6, and cancer development is also presented. Finally, L1-SIRT6 subnetwork SIRT6-PARP1-BRCA1/BRCA2-TRIM28-PIN1-p53 was constructed, where all nodes possess L1 retrotransposon activity-limiting activity and together represent candidates for multitarget control.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"101 ","pages":"Article 102496"},"PeriodicalIF":12.5,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142303175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroenergetic alterations in neurodegenerative diseases: A systematic review and meta-analysis of in vivo 31P-MRS studies","authors":"Yinghua Jing ,&nbsp;Alexa Haeger ,&nbsp;Fawzi Boumezbeur ,&nbsp;Ferdinand Binkofski ,&nbsp;Kathrin Reetz ,&nbsp;Sandro Romanzetti","doi":"10.1016/j.arr.2024.102488","DOIUrl":"10.1016/j.arr.2024.102488","url":null,"abstract":"<div><p>Phosphorus magnetic resonance spectroscopy (³¹P-MRS) is applied for non-invasive studies of neuroenergetic metabolism in neurodegenerative diseases. However, the findings are inconsistent and have not yet been tested in meta-analyses. To address this gap, we performed a systematic review of 29 studies and conducted meta-analyses for 9 studies on Alzheimer’s disease (AD, <em>n</em> = 140 patients), 9 studies on Parkinson’s disease (PD, <em>n</em> = 183 patients), 3 studies on Progressive Supranuclear Palsy (PSP, <em>n</em> = 42 patients), and 2 studies on Multiple System Atrophy (MSA, <em>n</em> = 24 patients). Compared to controls, AD patients had a higher ratio of phosphomonoesters/phosphodiesters (PME/PDE) in the frontal lobe (MD = 0.049, <em>p</em> = 0.0003); PD patients showed decreases in PME/PDE in the putamen (MD = -0.050, <em>p</em> = 0.023) and adenosine triphosphate/inorganic phosphate (ATP/Pi) in the midbrain (MD = -0.274, <em>p</em> = 0.002); PSP patients presented increased phosphocreatine (PCr)/Pi in the basal ganglia (MD = 0.556, <em>p</em> = 0.030) and adenosine diphosphate (ADP)/Pi in the occipital lobe (MD = 0.005, <em>p</em> = 0.009); no significant effects were observed in MSA. Here, our review underlines the importance of ³¹P-MRS in the characterization of distinct neuroenergetic changes and its potential to improve the diagnosis and follow-up of neurodegenerative diseases.</p></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"101 ","pages":"Article 102488"},"PeriodicalIF":12.5,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1568163724003064/pdfft?md5=1ba8da70fb91b4d89efcf568cff7722e&pid=1-s2.0-S1568163724003064-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142147038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The emerging role of exercise in Alzheimer’s disease: Focus on mitochondrial function","authors":"Lili Feng ,&nbsp;Bowen Li ,&nbsp;Su Sean Yong ,&nbsp;Xu Wen ,&nbsp;Zhenjun Tian","doi":"10.1016/j.arr.2024.102486","DOIUrl":"10.1016/j.arr.2024.102486","url":null,"abstract":"<div><div>Alzheimer’s disease (AD) is an age-related neurodegenerative disease characterized by memory impairment and cognitive dysfunction, which eventually leads to the disability and mortality of older adults. Although the precise mechanisms by which age promotes the development of AD remains poorly understood, mitochondrial dysfunction plays a central role in the development of AD. Currently, there is no effective treatment for this debilitating disease. It is well accepted that exercise exerts neuroprotective effects by ameliorating mitochondrial dysfunction in the neurons of AD, which involves multiple mechanisms, including mitochondrial dynamics, biogenesis, mitophagy, transport, and signal transduction. In addition, exercise promotes mitochondria communication with other organelles in AD neurons, which should receive more attentions in the future.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"101 ","pages":"Article 102486"},"PeriodicalIF":12.5,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142147039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Motoric cognitive risk syndrome as a predictive factor of cognitive impairment and dementia – A systematic review and meta-analysis","authors":"Nicholas E.-Kai Lim ,&nbsp;Brian Sheng Yep Yeo ,&nbsp;Rachel Siying Lee ,&nbsp;Jun Xiang Lim ,&nbsp;Yiong Huak Chan ,&nbsp;Nagaendran Kandiah ,&nbsp;Roger Ho ,&nbsp;Cyrus Su Hui Ho ,&nbsp;Jean Woo ,&nbsp;Hidenori Arai ,&nbsp;Reshma Aziz Merchant","doi":"10.1016/j.arr.2024.102470","DOIUrl":"10.1016/j.arr.2024.102470","url":null,"abstract":"<div><h3>Background</h3><p>Motoric cognitive risk syndrome (MCR) is defined as the presence of slow gait-speed and subjective cognitive decline in older individuals without mobility disability or dementia. While some studies suggest that MCR is a pre-dementia syndrome and may help predict the risk of cognitive impairment and dementia, not all studies concur. The objective of this study is to comprehensively summarize and synthesize evidence to assess the association between MCR and cognitive impairment and dementia.</p></div><div><h3>Methods</h3><p>Following a pre-specified protocol, two authors systematically searched PubMed, Embase, and The Cochrane Library from inception to 19 August 2024 for observational or randomized studies pertaining to the association between MCR and cognitive impairment and dementia. We favoured maximally adjusted hazards and odds ratios to determine the longitudinal and cross-sectional risk of cognitive impairment and dementia. We investigated for potential sources of heterogeneity and also conducted sensitivity and subgroup analyses by continent and the type of cognitive outcome. The quality of evidence was assessed using the Newcastle-Ottawa Scale (NOS) and the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) framework.</p></div><div><h3>Results</h3><p>We included 20 studies comprising a combined cohort of 1206,782 participants, of which 17 studies were included in the quantitative analysis. The pooled analysis outlined that individuals with MCR exhibited 2.20-fold higher risk of cognitive impairment and dementia, compared to controls (RR=2.20; 95 %CI=1.91–2.53). These findings remained robust across all subgroup analyses, sensitivity analyses and assessments of publication bias.</p></div><div><h3>Conclusion</h3><p>MCR may be considered a predictive factor for long-term cognitive impairment and dementia. This should be taken into consideration when clinically evaluating the risk of cognitive impairment and dementia but further research is required to lend greater clarity to this association.</p></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"101 ","pages":"Article 102470"},"PeriodicalIF":12.5,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142156915","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The influence of education in predicting conversion from Subjective cognitive decline (SCD) to objective cognitive impairment: A systematic review and meta-analysis","authors":"Sonali Arora ,&nbsp;Scott B. Patten ,&nbsp;Sabela C. Mallo ,&nbsp;Cristina Lojo-Seoane ,&nbsp;Alba Felpete ,&nbsp;David Facal-Mayo ,&nbsp;Arturo X. Pereiro","doi":"10.1016/j.arr.2024.102487","DOIUrl":"10.1016/j.arr.2024.102487","url":null,"abstract":"<div><h3>Background</h3><p>Subjective cognitive decline (SCD) is considered a pre-symptomatic stage of dementia characterized by cognitive complaints. The ability of education to reduce the risk of dementia is well known. Our objective is to investigate the influence of education on the risk of progression from SCD to MCI or dementia.</p></div><div><h3>Methods</h3><p>Prospective longitudinal studies of adults (≥50 years) with SCD evaluating progression to objective cognitive decline, MCI, or dementia were selected. Pooled estimates (random effects model) and 95 % confidence intervals were calculated, exploring heterogeneity. Standardized education differences, Odds Ratio, or Hazard Ratio between converters and non-converters were estimated.</p></div><div><h3>Results</h3><p>The systematic review carried out showed that high education, as well as other cognitive reserve proxies, delays cognitive decline. The first meta-analysis showed a significant association of SCD with conversion in both high and low education strata. A second meta-analysis considering education as a continuous variable found that SCD converters showed two years less education than non-converters.</p></div><div><h3>Conclusions</h3><p>Our results suggest that education has a delaying effect against cognitive decline progression. The presumed improvement in accurately detecting cognitive decline associated with better metacognitive skills in higher-educated SCD participants does not seem to neutralize the incremental risk of objective cognitive decline associated with lower educational attainment.</p></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"101 ","pages":"Article 102487"},"PeriodicalIF":12.5,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1568163724003052/pdfft?md5=11063903a9b90f09eb23bd22a0ad3508&pid=1-s2.0-S1568163724003052-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142147040","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of metal ions in stroke: Current evidence and future perspectives","authors":"Shaoshuai Wang ,&nbsp;Mengzhe Qin ,&nbsp;Xiaochong Fan ,&nbsp;Chao Jiang ,&nbsp;Qingchuan Hou ,&nbsp;Ziyi Ye ,&nbsp;Xinru Zhang ,&nbsp;Yunfan Yang ,&nbsp;Jingyu Xiao ,&nbsp;Kevin Wallace ,&nbsp;Yousef Rastegar-Kashkooli ,&nbsp;Qinfeng Peng ,&nbsp;Dongqi Jin ,&nbsp;Junyang Wang ,&nbsp;Menglu Wang ,&nbsp;Ruoqi Ding ,&nbsp;Jin Tao ,&nbsp;Yun Tai Kim ,&nbsp;Ujjal K. Bhawal ,&nbsp;Junmin Wang ,&nbsp;Jian Wang","doi":"10.1016/j.arr.2024.102498","DOIUrl":"10.1016/j.arr.2024.102498","url":null,"abstract":"<div><p>Metal ions play a pivotal role in maintaining optimal brain function within the human body. Nevertheless, the accumulation of these ions can result in irregularities that lead to brain damage and dysfunction. Disruptions of metal ion homeostasis can result in various pathologies, including inflammation, redox dysregulation, and blood-brain barrier disruption. While research on metal ions has chiefly focused on neurodegenerative diseases, little attention has been given to their involvement in the onset and progression of stroke. Recent studies have identified cuproptosis and confirmed ferroptosis as significant factors in stroke pathology, underscoring the importance of metal ions in stroke pathology, including abnormal ion transport, neurotoxicity, blood-brain barrier damage, and cell death. Additionally, it provides an overview of contemporary metal ion chelators and detection techniques, which may offer novel approaches to stroke treatment.</p></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"101 ","pages":"Article 102498"},"PeriodicalIF":12.5,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142147041","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CSF and blood glial fibrillary acidic protein for the diagnosis of Alzheimer's disease: A systematic review and meta-analysis","authors":"Yutong Zou ,&nbsp;Yifei Wang ,&nbsp;Xiaoli Ma ,&nbsp;Danni Mu ,&nbsp;Jian Zhong ,&nbsp;Chaochao Ma ,&nbsp;Chenhui Mao ,&nbsp;Songlin Yu ,&nbsp;Jing Gao ,&nbsp;Ling Qiu","doi":"10.1016/j.arr.2024.102485","DOIUrl":"10.1016/j.arr.2024.102485","url":null,"abstract":"<div><p>Recently included in the 2024 new revised diagnostic criteria of Alzheimer’s disease (AD), glial fibrillary acidic protein (GFAP) has garnered significant attention. A systematic review and meta-analysis were performed to comprehensively evaluate the diagnostic, differential diagnostic, and prospective diagnostic performance of GFAP in cerebrospinal fluid (CSF) and blood for AD continuum. A literature search using common electronic databases, important websites and historical search way was performed from inception to the beginning of March 2023. The inclusion criteria was studies evaluating the diagnostic accuracy of GFAP in CSF and/or blood for the AD continuum patients, utilizing PET scans, CSF biomarkers and/or clinical criteria. The systematic review and meta-analysis were conducted referring to the Cochrane Handbook. In total, 34 articles were eventually included in the meta-analysis, 29 of which were published within the past three years. Blood GFAP exhibited good diagnostic accuracy across various AD continuum patients, and the summary area under curve for distinguishing PET positive and negative individuals, CSF biomarkers defined positive and negative individuals, clinically diagnosed AD and cognitive unimpaired controls, AD and/or mild cognitive impairment and other neurological diseases, and prospective cases and controls was 0.85[0.81–0.88], 0.77[0.73–0.81], 0.92[0.90–0.94], 0.80[0.77–0.84], and 0.79[0.75–0.82], respectively. Only several studies were recognized to evaluate the diagnostic accuracy of CSF GFAP, which was not as good as that of blood GFAP (paired mixed data: AUC = 0.86 vs. AUC = 0.77), but its accuracy remarkably increased to AUC = 0.91 when combined with other factors like sex, age, and ApoE genotype. In summary, GFAP, particularly in blood, shown good diagnostic, differential diagnostic, and prospective diagnostic accuracy for AD continuum patients, with improved accuracy when used alongside other basic indexes.</p></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"101 ","pages":"Article 102485"},"PeriodicalIF":12.5,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142142000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Imidazoline receptors as a new therapeutic target in Huntington’s disease: A preclinical overview","authors":"Sakshi Jari,&nbsp;Nandini Ratne,&nbsp;Manasi Tadas,&nbsp;Raj Katariya,&nbsp;Mayur Kale,&nbsp;Milind Umekar,&nbsp;Brijesh Taksande","doi":"10.1016/j.arr.2024.102482","DOIUrl":"10.1016/j.arr.2024.102482","url":null,"abstract":"<div><p>An autosomal dominant neurodegenerative disease called Huntington's disease (HD) is characterized by motor dysfunction, cognitive decline, and a variety of psychiatric symptoms due to the expansion of polyglutamine in the Huntingtin gene. The disease primarily affects the striatal neurons within the basal ganglia, leading to significant neuronal loss and associated symptoms such as chorea and dystonia. Current therapeutic approaches focus on symptom management without altering the disease's progression, highlighting a pressing need for novel treatment strategies. Recent studies have identified imidazoline receptors (IRs) as promising targets for neuroprotective and disease-modifying interventions in HD. IRs, particularly the I1 and I2 subtypes, are involved in critical physiological processes such as neurotransmission, neuronal excitability, and cell survival. Activation of these receptors has been shown to modulate neurotransmitter release and provide neuroprotective effects in preclinical models of neurodegeneration. This review discusses the potential of IR-targeted therapies to not only alleviate multiple symptoms of HD but also possibly slow the progression of the disease. We emphasize the necessity for ongoing research to further elucidate the role of IRs in HD and develop selective ligands that could lead to effective and safe treatments, thereby significantly improving patient outcomes and quality of life.</p></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"101 ","pages":"Article 102482"},"PeriodicalIF":12.5,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142142016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pathogenesis, diagnostics, and therapeutics for Alzheimer's disease: Breaking the memory barrier","authors":"Pushpa Tryphena Kamatham ,&nbsp;Rashi Shukla ,&nbsp;Dharmendra Kumar Khatri ,&nbsp;Lalitkumar K. Vora","doi":"10.1016/j.arr.2024.102481","DOIUrl":"10.1016/j.arr.2024.102481","url":null,"abstract":"<div><p>Alzheimer's disease (AD) is the most common cause of dementia and accounts for 60–70 % of all cases. It affects millions of people worldwide. AD poses a substantial economic burden on societies and healthcare systems. AD is a progressive neurodegenerative disorder characterized by cognitive decline, memory loss, and impaired daily functioning. As the prevalence of AD continues to increase, understanding its pathogenesis, improving diagnostic methods, and developing effective therapeutics have become paramount. This comprehensive review delves into the intricate mechanisms underlying AD, explores the current state of diagnostic techniques, and examines emerging therapeutic strategies. By revealing the complexities of AD, this review aims to contribute to the growing body of knowledge surrounding this devastating disease.</p></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"101 ","pages":"Article 102481"},"PeriodicalIF":12.5,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S156816372400299X/pdfft?md5=d59f1b7843c16130db5766f8f73af5cf&pid=1-s2.0-S156816372400299X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142142003","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}