Pub Date : 2024-09-19DOI: 10.1016/j.arr.2024.102509
Carmelo Luca Smeralda , Siddhartha Pandit , Sonia Turrini , Julianne Reilly , Annalisa Palmisano , Giulia Sprugnoli , Harald Hampel , Alberto Benussi , Barbara Borroni , Daniel Press , Alexander Rotenberg , Georges El Fakhri , Giacomo Koch , Simone Rossi , Emiliano Santarnecchi
Parvalbumin-positive (PV+) basket neurons are fast-spiking, non-adapting inhibitory interneurons whose oscillatory activity is essential for regulating cortical excitation/inhibition balance. Their dysfunction results in cortical hyperexcitability and gamma rhythm disruption, which have recently gained substantial traction as contributing factors as well as potential therapeutic targets for the treatment of Alzheimer’s Disease (AD). Recent evidence indicates that PV+ cells are also impaired in Frontotemporal Dementia (FTD) and Dementia with Lewy bodies (DLB). However, no attempt has been made to integrate these findings into a coherent pathophysiological framework addressing the contribution of PV+ interneuron dysfunction to the generation of cortical hyperexcitability and gamma rhythm disruption in FTD and DLB. To fill this gap, we epitomized the most recent evidence on PV+ interneuron impairment in AD, FTD, and DLB, focusing on its contribution to the generation of cortical hyperexcitability and gamma oscillatory disruption and their interplay with misfolded protein accumulation, neuronal death, and clinical symptoms’ onset. Our work deepens the current understanding concerning the role of PV+ interneuron dysfunction across neurodegenerative dementias, highlighting commonalities and differences among AD, FTD, and DLB, thus paving the way for identifying novel biomarkers and potential therapeutic targets for the treatment of these diseases.
{"title":"The role of parvalbumin interneuron dysfunction across neurodegenerative dementias","authors":"Carmelo Luca Smeralda , Siddhartha Pandit , Sonia Turrini , Julianne Reilly , Annalisa Palmisano , Giulia Sprugnoli , Harald Hampel , Alberto Benussi , Barbara Borroni , Daniel Press , Alexander Rotenberg , Georges El Fakhri , Giacomo Koch , Simone Rossi , Emiliano Santarnecchi","doi":"10.1016/j.arr.2024.102509","DOIUrl":"10.1016/j.arr.2024.102509","url":null,"abstract":"<div><div>Parvalbumin-positive (PV+) basket neurons are fast-spiking, non-adapting inhibitory interneurons whose oscillatory activity is essential for regulating cortical excitation/inhibition balance. Their dysfunction results in cortical hyperexcitability and gamma rhythm disruption, which have recently gained substantial traction as contributing factors as well as potential therapeutic targets for the treatment of Alzheimer’s Disease (AD). Recent evidence indicates that PV+ cells are also impaired in Frontotemporal Dementia (FTD) and Dementia with Lewy bodies (DLB). However, no attempt has been made to integrate these findings into a coherent pathophysiological framework addressing the contribution of PV+ interneuron dysfunction to the generation of cortical hyperexcitability and gamma rhythm disruption in FTD and DLB. To fill this gap, we epitomized the most recent evidence on PV+ interneuron impairment in AD, FTD, and DLB, focusing on its contribution to the generation of cortical hyperexcitability and gamma oscillatory disruption and their interplay with misfolded protein accumulation, neuronal death, and clinical symptoms’ onset. Our work deepens the current understanding concerning the role of PV+ interneuron dysfunction across neurodegenerative dementias, highlighting commonalities and differences among AD, FTD, and DLB, thus paving the way for identifying novel biomarkers and potential therapeutic targets for the treatment of these diseases.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"101 ","pages":"Article 102509"},"PeriodicalIF":12.5,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142303158","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}
Pub Date : 2024-09-19DOI: 10.1016/j.arr.2024.102506
Nurul Izzati Ahmad Fadzuli , Siong Meng Lim , Chin Fen Neoh , Abu Bakar Abdul Majeed , Maw Pin Tan , Hui Min Khor , Ai Huey Tan , Kalavathy Ramasamy
This systematic review and meta-analysis appraised previous findings to uncover potential faecal intestinal permeability and intestinal inflammatory markers in older adults. A comprehensive literature search led to the identification of ten eligible studies with findings of potential faecal intestinal permeability (zonulin and alpha-1-antitrypsin) and intestinal inflammatory markers [calprotectin, lactoferrin and neutrophil gelatinase-associated lipocalin (NGAL)]. Most of the cases (n > 2) [Parkinson’s disease (PD) and Alzheimer’s disease (AD)] exhibited higher faecal alpha-1-antitrypsin, zonulin and calprotectin levels. The present meta-analysis confirmed significantly higher faecal alpha-1-antitrypsin in older persons with PD compared to non-PD [MD = 22.92 mg/dL; 95 % CI = 14.02–31.81, p < 0.00001; I2 = 0 % (p = 0.73)]. There was, however, no significant difference in faecal zonulin between PD and non-PD individuals [MD = 26.88 ng/mL; 95 % CI = −29.26–83.01, p = 0.35; I2 = 94 % (p < 0.0001)]. Meanwhile, faecal calprotectin was higher in older adults with GI symptoms, multiple system atrophy (MSA) or PD than the healthy controls [MD = 9.51 μg/g; 95 % CI = 0.07–18.95, p = 0.05; I2 = 84 % (p < 0.00001)]. Altogether, faecal calprotectin appears to be a potential intestinal inflammatory marker whereas previous findings on faecal alpha-1-antitrypsin as an intestinal permeability marker remain limited and require further validation.
本系统综述和荟萃分析对以往的研究结果进行了评估，以发现老年人潜在的粪便肠道渗透性和肠道炎症标志物。通过全面的文献检索，确定了十项符合条件的研究，这些研究发现了潜在的粪便肠道通透性（zonulin 和 alpha-1-抗胰蛋白酶）和肠道炎症标记物[钙蛋白、乳铁蛋白和中性粒细胞明胶酶相关脂联素（NGAL）]。大多数病例（n > 2）[帕金森病（PD）和阿尔茨海默病（AD）]的粪便中α-1-抗胰蛋白酶、zonulin 和钙蛋白水平较高。本荟萃分析证实，与非帕金森病患者相比，帕金森病老年人粪便中的α-1-抗胰蛋白酶水平明显更高[MD = 22.92mg/dL; 95% CI = 14.02 to 31.81, p < 0.00001; I2 = 0% (p = 0.73)]。然而，腹水症患者和非腹水症患者粪便中的zonulin没有明显差异[MD = 26.88ng/mL; 95% CI = -29.26 to 83.01, p = 0.35; I2 = 94% (p < 0.0001)]。同时，与健康对照组相比，有消化道症状、多系统萎缩（MSA）或腹膜后疾病的老年人的粪便钙蛋白更高[MD = 9.51μg/g；95% CI = 0.07 to 18.95，p = 0.05；I2 = 84% (p < 0.00001)]。总之，粪便钙蛋白似乎是一种潜在的肠道炎症标志物，而之前关于粪便α-1-抗胰蛋白酶作为肠道通透性标志物的研究结果仍然有限，需要进一步验证。
{"title":"Faecal intestinal permeability and intestinal inflammatory markers in older adults with age-related disorders: A systematic review and meta-analysis","authors":"Nurul Izzati Ahmad Fadzuli , Siong Meng Lim , Chin Fen Neoh , Abu Bakar Abdul Majeed , Maw Pin Tan , Hui Min Khor , Ai Huey Tan , Kalavathy Ramasamy","doi":"10.1016/j.arr.2024.102506","DOIUrl":"10.1016/j.arr.2024.102506","url":null,"abstract":"<div><div>This systematic review and meta-analysis appraised previous findings to uncover potential faecal intestinal permeability and intestinal inflammatory markers in older adults. A comprehensive literature search led to the identification of ten eligible studies with findings of potential faecal intestinal permeability (zonulin and alpha-1-antitrypsin) and intestinal inflammatory markers [calprotectin, lactoferrin and neutrophil gelatinase-associated lipocalin (NGAL)]. Most of the cases (n <u>></u> 2) [Parkinson’s disease (PD) and Alzheimer’s disease (AD)] exhibited higher faecal alpha-1-antitrypsin, zonulin and calprotectin levels. The present meta-analysis confirmed significantly higher faecal alpha-1-antitrypsin in older persons with PD compared to non-PD [MD = 22.92 mg/dL; 95 % CI = 14.02–31.81, <em>p</em> < 0.00001; I<sup>2</sup> = 0 % (<em>p</em> = 0.73)]. There was, however, no significant difference in faecal zonulin between PD and non-PD individuals [MD = 26.88 ng/mL; 95 % CI = −29.26–83.01, <em>p</em> = 0.35; I<sup>2</sup> = 94 % (<em>p</em> < 0.0001)]. Meanwhile, faecal calprotectin was higher in older adults with GI symptoms, multiple system atrophy (MSA) or PD than the healthy controls [MD = 9.51 μg/g; 95 % CI = 0.07–18.95, <em>p</em> = 0.05; I<sup>2</sup> = 84 % (<em>p</em> < 0.00001)]. Altogether, faecal calprotectin appears to be a potential intestinal inflammatory marker whereas previous findings on faecal alpha-1-antitrypsin as an intestinal permeability marker remain limited and require further validation.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"101 ","pages":"Article 102506"},"PeriodicalIF":12.5,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142303173","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}
Pub Date : 2024-09-19DOI: 10.1016/j.arr.2024.102508
Hong Liu , Mengyuan Wu , Haoyu Huang , Xiaolin Chen , Peiling Zeng , Ying Xu
Background
Mild cognitive impairment (MCI) is a critical time window for implementing prevention strategies to attenuate or delay cognitive decline. Non-invasive brain stimulation (NIBS) techniques are promising non-pharmacological therapies for improving the cognitive function of MCI, but it is unclear which type of NIBS protocol is most effective. This study aimed to compare and rank the beneficial effect of different NIBS methods/protocols on cognitive function and examine the acceptability of NIBS in patients with MCI.
Methods
Electronic search of PubMed, Cochrane Library, EMBASE, China National Knowledge Infrastructure, Wanfang Database, and Chongqing VIP Database up to November 2023. Patients with diagnosis of MCI were included. The primary outcomes were acceptability and pre-post treatment changes in global cognitive function, and the secondary outcomes were specific cognitive domains (language and executive function). All network meta‑analysis procedures were performed under the frequentist model. A protocol for this systematic review was registered in PROSPERO (Registration number: CRD42023441448).
Results
A network meta-analysis was conducted on 19 eligible RCTs consisting of 599 subjects. Compared with the sham stimulation, Repetitive Transcranial Magnetic Stimulation over the Bilateral dorsolateral prefrontal cortex (rTMS-F3F4) showed the strongest improvement in global cognitive function in MCI patients (SMD =1.52[95 %CIs =0.49–2.56]), followed by rTMS over the left dorsolateral prefrontal cortex (rTMS-F3) (SMD =1.25[95 %CIs =0.57–1.93]); Moreover, rTMS-F3F4 showed more significant efficacy in language function (SMD =0.96[95 %CIs = 0.20–1.72]); No statistically significant differences were found among the other cognitive domains. Compared with the rTMS-F4, rTMS-F3F4 showed a stronger improvement in global cognitive function in MCI patients (SMD =1.80[95 %CIs =0.02–3.59]). Similar results were obtained in subgroup analyses of cognitive function. All the methods were well-tolerated with an acceptable safety profile.
Conclusion
The present findings provide evidence of the benefits of NIBS, especially TMS stimulating the bilateral dorsolateral prefrontal cortex, for the beneficial effect on cognitive and language function in patients with MCI. However, because few studies were available for inclusion, additional well-designed, large-scale RCTs are warranted to support exploring longer-term dynamic effects.
{"title":"Comparative efficacy of non-invasive brain stimulation on cognition function in patients with mild cognitive impairment: A systematic review and network meta-analysis","authors":"Hong Liu , Mengyuan Wu , Haoyu Huang , Xiaolin Chen , Peiling Zeng , Ying Xu","doi":"10.1016/j.arr.2024.102508","DOIUrl":"10.1016/j.arr.2024.102508","url":null,"abstract":"<div><h3>Background</h3><div>Mild cognitive impairment (MCI) is a critical time window for implementing prevention strategies to attenuate or delay cognitive decline. Non-invasive brain stimulation (NIBS) techniques are promising non-pharmacological therapies for improving the cognitive function of MCI, but it is unclear which type of NIBS protocol is most effective. This study aimed to compare and rank the beneficial effect of different NIBS methods/protocols on cognitive function and examine the acceptability of NIBS in patients with MCI.</div></div><div><h3>Methods</h3><div>Electronic search of PubMed, Cochrane Library, EMBASE, China National Knowledge Infrastructure, Wanfang Database, and Chongqing VIP Database up to November 2023. Patients with diagnosis of MCI were included. The primary outcomes were acceptability and pre-post treatment changes in global cognitive function, and the secondary outcomes were specific cognitive domains (language and executive function). All network meta‑analysis procedures were performed under the frequentist model. A protocol for this systematic review was registered in PROSPERO (Registration number: CRD42023441448).</div></div><div><h3>Results</h3><div>A network meta-analysis was conducted on 19 eligible RCTs consisting of 599 subjects. Compared with the sham stimulation, Repetitive Transcranial Magnetic Stimulation over the Bilateral dorsolateral prefrontal cortex (rTMS-F3F4) showed the strongest improvement in global cognitive function in MCI patients (SMD =1.52[95 %CIs =0.49–2.56]), followed by rTMS over the left dorsolateral prefrontal cortex (rTMS-F3) (SMD =1.25[95 %CIs =0.57–1.93]); Moreover, rTMS-F3F4 showed more significant efficacy in language function (SMD =0.96[95 %CIs = 0.20–1.72]); No statistically significant differences were found among the other cognitive domains. Compared with the rTMS-F4, rTMS-F3F4 showed a stronger improvement in global cognitive function in MCI patients (SMD =1.80[95 %CIs =0.02–3.59]). Similar results were obtained in subgroup analyses of cognitive function. All the methods were well-tolerated with an acceptable safety profile.</div></div><div><h3>Conclusion</h3><div>The present findings provide evidence of the benefits of NIBS, especially TMS stimulating the bilateral dorsolateral prefrontal cortex, for the beneficial effect on cognitive and language function in patients with MCI. However, because few studies were available for inclusion, additional well-designed, large-scale RCTs are warranted to support exploring longer-term dynamic effects.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"101 ","pages":"Article 102508"},"PeriodicalIF":12.5,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142303171","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}
Pub Date : 2024-09-19DOI: 10.1016/j.arr.2024.102507
Wei-en Wang , Breton M. Asken , Jesse C. DeSimone , Shellie-Anne Levy , Warren Barker , Jacob A. Fiala , Idaly Velez-Uribe , Rosie E. Curiel Cid , Monica Rósselli , Michael Marsiske , Malek Adjouadi , David A. Loewenstein , Ranjan Duara , Glenn E. Smith , Melissa J. Armstrong , Lisa L. Barnes , David E. Vaillancourt , Stephen A. Coombes
Neuroimaging and biofluid biomarkers provide a proxy of pathological changes for Alzheimer’s disease (AD) and are useful in improving diagnosis and assessing disease progression. However, it is not clear how race/ethnicity and different prevalence of AD risks impact biomarker levels. In this narrative review, we survey studies focusing on comparing biomarker differences between non-Hispanic White American(s) (NHW), African American(s) (AA), Hispanic/Latino American(s) (HLA), and Asian American(s) with normal cognition, mild cognitive impairment, and dementia. We found no strong evidence of racial and ethnic differences in imaging biomarkers after controlling for cognitive status and cardiovascular risks. For biofluid biomarkers, in AA, higher levels of plasma Aβ42/Aβ40, and lower levels of CSF total tau and p-tau 181, were observed after controlling for APOE status and comorbidities compared to NHW. Examining the impact of AD risks and comorbidities on biomarkers and their contributions to racial/ethnic differences in cognitive impairment are critical to interpreting biomarkers, understanding their generalizability, and eliminating racial/ethnic health disparities.
{"title":"Neuroimaging and biofluid biomarkers across race and ethnicity in older adults across the spectrum of cognition","authors":"Wei-en Wang , Breton M. Asken , Jesse C. DeSimone , Shellie-Anne Levy , Warren Barker , Jacob A. Fiala , Idaly Velez-Uribe , Rosie E. Curiel Cid , Monica Rósselli , Michael Marsiske , Malek Adjouadi , David A. Loewenstein , Ranjan Duara , Glenn E. Smith , Melissa J. Armstrong , Lisa L. Barnes , David E. Vaillancourt , Stephen A. Coombes","doi":"10.1016/j.arr.2024.102507","DOIUrl":"10.1016/j.arr.2024.102507","url":null,"abstract":"<div><div>Neuroimaging and biofluid biomarkers provide a proxy of pathological changes for Alzheimer’s disease (AD) and are useful in improving diagnosis and assessing disease progression. However, it is not clear how race/ethnicity and different prevalence of AD risks impact biomarker levels. In this narrative review, we survey studies focusing on comparing biomarker differences between non-Hispanic White American(s) (NHW), African American(s) (AA), Hispanic/Latino American(s) (HLA), and Asian American(s) with normal cognition, mild cognitive impairment, and dementia. We found no strong evidence of racial and ethnic differences in imaging biomarkers after controlling for cognitive status and cardiovascular risks. For biofluid biomarkers, in AA, higher levels of plasma Aβ42/Aβ40, and lower levels of CSF total tau and p-tau 181, were observed after controlling for <em>APOE</em> status and comorbidities compared to NHW. Examining the impact of AD risks and comorbidities on biomarkers and their contributions to racial/ethnic differences in cognitive impairment are critical to interpreting biomarkers, understanding their generalizability, and eliminating racial/ethnic health disparities.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"101 ","pages":"Article 102507"},"PeriodicalIF":12.5,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142303174","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}
Higher levels of pulse wave velocity (PWV) have been related with the presence of small vessel disease that could damage the brain, in which white matter hyperintensities (WMH) could be presented as consequence. This meta-analysis aims to examine the cross-sectional and longitudinal associations between PWV and the presence of WMH among older adults.
Methods
We searched PubMed, Scopus, and WOS until June 2024. Pooled Odds Ratio (p-OR) were estimated for the cross-sectional and longitudinal associations between PWV and WMH. In addition, we explored whether this associations could be modified by type of PWV measurement and study and sample characteristics.
Results
The p-OR between PWV and WMH was 1.16 (95 % CI, 1.10–1.22) for the cross-sectional and 1.07 (95 %, 1.00–1.15) for the longitudinal association. Similar figures were found by type of PWV measurement and no one of the explored characteristics modified this associations.
Conclusions
This meta-analysis revealed that the presence in and the long-term development of WMHs among older adults are more likely among those with elevated PWV.
{"title":"Association between pulse wave velocity and white matter hyperintensities among older adults: A meta-analysis of cross-sectional and longitudinal studies","authors":"Celia Álvarez-Bueno , María Medrano , Maribel Lucerón-Lucas-Torres , Iris Otero-Luis , Samuel López-López , Carla Geovanna Lever-Megina , Iván Cavero-Redondo","doi":"10.1016/j.arr.2024.102501","DOIUrl":"10.1016/j.arr.2024.102501","url":null,"abstract":"<div><h3>Background</h3><div>Higher levels of pulse wave velocity (PWV) have been related with the presence of small vessel disease that could damage the brain, in which white matter hyperintensities (WMH) could be presented as consequence. This meta-analysis aims to examine the cross-sectional and longitudinal associations between PWV and the presence of WMH among older adults.</div></div><div><h3>Methods</h3><div>We searched PubMed, Scopus, and WOS until June 2024. Pooled Odds Ratio (p-OR) were estimated for the cross-sectional and longitudinal associations between PWV and WMH. In addition, we explored whether this associations could be modified by type of PWV measurement and study and sample characteristics.</div></div><div><h3>Results</h3><div>The p-OR between PWV and WMH was 1.16 (95 % CI, 1.10–1.22) for the cross-sectional and 1.07 (95 %, 1.00–1.15) for the longitudinal association. Similar figures were found by type of PWV measurement and no one of the explored characteristics modified this associations.</div></div><div><h3>Conclusions</h3><div>This meta-analysis revealed that the presence in and the long-term development of WMHs among older adults are more likely among those with elevated PWV.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"101 ","pages":"Article 102501"},"PeriodicalIF":12.5,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142303170","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}
Alzheimer’s disease (AD) presents a significant challenge in neurodegenerative research and clinical practice due to its complex etiology and progressive nature. The integration of artificial intelligence (AI) into the diagnosis, treatment, and prognostic modelling of AD holds promising potential to transform the landscape of dementia care. This review explores recent advancements in AI applications across various stages of AD management. In early diagnosis, AI-enhanced neuroimaging techniques, including MRI, PET, and CT scans, enable precise detection of AD biomarkers. Machine learning models analyze these images to identify patterns indicative of early cognitive decline. Additionally, AI algorithms are employed to detect genetic and proteomic biomarkers, facilitating early intervention. Cognitive and behavioral assessments have also benefited from AI, with tools that enhance the accuracy of neuropsychological tests and analyze speech and language patterns for early signs of dementia. Personalized treatment strategies have been revolutionized by AI-driven approaches. In drug discovery, virtual screening and drug repurposing, guided by predictive modelling, accelerate the identification of effective treatments. AI also aids in tailoring therapeutic interventions by predicting individual responses to treatments and monitoring patient progress, allowing for dynamic adjustment of care plans. Prognostic modelling, another critical area, utilizes AI to predict disease progression through longitudinal data analysis and risk prediction models. The integration of multi-modal data, combining clinical, genetic, and imaging information, enhances the accuracy of these predictions. Deep learning techniques are particularly effective in fusing diverse data types to uncover new insights into disease mechanisms and progression. Despite these advancements, challenges remain, including ethical considerations, data privacy, and the need for seamless integration of AI tools into clinical workflows. This review underscores the transformative potential of AI in AD management while highlighting areas for future research and development. By leveraging AI, the healthcare community can improve early diagnosis, personalize treatments, and predict disease outcomes more accurately, ultimately enhancing the quality of life for individuals with AD.
{"title":"AI-driven innovations in Alzheimer's disease: Integrating early diagnosis, personalized treatment, and prognostic modelling","authors":"Mayur Kale , Nitu Wankhede , Rupali Pawar , Suhas Ballal , Rohit Kumawat , Manish Goswami , Mohammad Khalid , Brijesh Taksande , Aman Upaganlawar , Milind Umekar , Spandana Rajendra Kopalli , Sushruta Koppula","doi":"10.1016/j.arr.2024.102497","DOIUrl":"10.1016/j.arr.2024.102497","url":null,"abstract":"<div><div>Alzheimer’s disease (AD) presents a significant challenge in neurodegenerative research and clinical practice due to its complex etiology and progressive nature. The integration of artificial intelligence (AI) into the diagnosis, treatment, and prognostic modelling of AD holds promising potential to transform the landscape of dementia care. This review explores recent advancements in AI applications across various stages of AD management. In early diagnosis, AI-enhanced neuroimaging techniques, including MRI, PET, and CT scans, enable precise detection of AD biomarkers. Machine learning models analyze these images to identify patterns indicative of early cognitive decline. Additionally, AI algorithms are employed to detect genetic and proteomic biomarkers, facilitating early intervention. Cognitive and behavioral assessments have also benefited from AI, with tools that enhance the accuracy of neuropsychological tests and analyze speech and language patterns for early signs of dementia. Personalized treatment strategies have been revolutionized by AI-driven approaches. In drug discovery, virtual screening and drug repurposing, guided by predictive modelling, accelerate the identification of effective treatments. AI also aids in tailoring therapeutic interventions by predicting individual responses to treatments and monitoring patient progress, allowing for dynamic adjustment of care plans. Prognostic modelling, another critical area, utilizes AI to predict disease progression through longitudinal data analysis and risk prediction models. The integration of multi-modal data, combining clinical, genetic, and imaging information, enhances the accuracy of these predictions. Deep learning techniques are particularly effective in fusing diverse data types to uncover new insights into disease mechanisms and progression. Despite these advancements, challenges remain, including ethical considerations, data privacy, and the need for seamless integration of AI tools into clinical workflows. This review underscores the transformative potential of AI in AD management while highlighting areas for future research and development. By leveraging AI, the healthcare community can improve early diagnosis, personalize treatments, and predict disease outcomes more accurately, ultimately enhancing the quality of life for individuals with AD.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"101 ","pages":"Article 102497"},"PeriodicalIF":12.5,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142303169","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}
Pub Date : 2024-09-14DOI: 10.1016/j.arr.2024.102503
Sang Gyun Noh , Hyun Woo Kim , Seungwoo Kim , Ki Wung Chung , Young-Suk Jung , Jeong-Hyun Yoon , Byung Pal Yu , Jaewon Lee , Hae Young Chung
Senoinflammation is characterized by an unresolved low-grade inflammatory process that affects multiple organs and systemic functions. This review begins with a brief overview of the fundamental concepts and frameworks of senoinflammation. It is widely involved in the aging of various organs and ultimately leads to progressive systemic degeneration. Senoinflammation underlying age-related inflammation, is causally related to metabolic dysregulation and the formation of senescence-associated secretory phenotype (SASP) during aging and age-related diseases. This review discusses the biochemical evidence and molecular biology data supporting the concept of senoinflammation and its regulatory processes, highlighting the anti-aging and anti-inflammatory effects of calorie restriction (CR). Experimental data from CR studies demonstrated effective suppression of various pro-inflammatory cytokines and chemokines, lipid accumulation, and SASP during aging. In conclusion, senoinflammation represents the basic mechanism that creates a microenvironment conducive to aging and age-related diseases. Furthermore, it serves as a potential therapeutic target for mitigating aging and age-related diseases.
{"title":"Senoinflammation as the underlying mechanism of aging and its modulation by calorie restriction","authors":"Sang Gyun Noh , Hyun Woo Kim , Seungwoo Kim , Ki Wung Chung , Young-Suk Jung , Jeong-Hyun Yoon , Byung Pal Yu , Jaewon Lee , Hae Young Chung","doi":"10.1016/j.arr.2024.102503","DOIUrl":"10.1016/j.arr.2024.102503","url":null,"abstract":"<div><p>Senoinflammation is characterized by an unresolved low-grade inflammatory process that affects multiple organs and systemic functions. This review begins with a brief overview of the fundamental concepts and frameworks of senoinflammation. It is widely involved in the aging of various organs and ultimately leads to progressive systemic degeneration. Senoinflammation underlying age-related inflammation, is causally related to metabolic dysregulation and the formation of senescence-associated secretory phenotype (SASP) during aging and age-related diseases. This review discusses the biochemical evidence and molecular biology data supporting the concept of senoinflammation and its regulatory processes, highlighting the anti-aging and anti-inflammatory effects of calorie restriction (CR). Experimental data from CR studies demonstrated effective suppression of various pro-inflammatory cytokines and chemokines, lipid accumulation, and SASP during aging. In conclusion, senoinflammation represents the basic mechanism that creates a microenvironment conducive to aging and age-related diseases. Furthermore, it serves as a potential therapeutic target for mitigating aging and age-related diseases.</p></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"101 ","pages":"Article 102503"},"PeriodicalIF":12.5,"publicationDate":"2024-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142272817","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}
Pub Date : 2024-09-14DOI: 10.1016/j.arr.2024.102461
Carol Holland , Nikolett Dravecz , Lauren Owens , Alexandre Benedetto , Irundika Dias , Alan Gow , Susan Broughton
Cognitive frailty (CF) is the conjunction of cognitive impairment without dementia and physical frailty. While predictors of each element are well-researched, mechanisms of their co-occurrence have not been integrated, particularly in terms of relationships between social, psychological, and biological factors. This interdisciplinary scoping review set out to categorise a heterogenous multidisciplinary literature to identify potential pathways and mechanisms of CF, and research gaps. Studies were included if they used the definition of CF OR focused on conjunction of cognitive impairment and frailty (by any measure), AND excluded studies on specific disease populations, interventions, epidemiology or prediction of mortality. Searches used Web of Science, PubMed and Science Direct. Search terms included “cognitive frailty” OR ((“cognitive decline” OR “cognitive impairment”) AND (frail*)), with terms to elicit mechanisms, predictors, causes, pathways and risk factors. To ensure inclusion of animal and cell models, keywords such as “behavioural” or “cognitive decline” or “senescence”, were added. 206 papers were included. Descriptive analysis provided high-level categorisation of determinants from social and environmental through psychological to biological. Patterns distinguishing CF from Alzheimer’s disease were identified and social and psychological moderators and mediators of underlying biological and physiological changes and of trajectories of CF development were suggested as foci for further research.
{"title":"Understanding exogenous factors and biological mechanisms for cognitive frailty: A multidisciplinary scoping review","authors":"Carol Holland , Nikolett Dravecz , Lauren Owens , Alexandre Benedetto , Irundika Dias , Alan Gow , Susan Broughton","doi":"10.1016/j.arr.2024.102461","DOIUrl":"10.1016/j.arr.2024.102461","url":null,"abstract":"<div><p>Cognitive frailty (CF) is the conjunction of cognitive impairment without dementia and physical frailty. While predictors of each element are well-researched, mechanisms of their co-occurrence have not been integrated, particularly in terms of relationships between social, psychological, and biological factors. This interdisciplinary scoping review set out to categorise a heterogenous multidisciplinary literature to identify potential pathways and mechanisms of CF, and research gaps. Studies were included if they used the definition of CF OR focused on conjunction of cognitive impairment and frailty (by any measure), AND excluded studies on specific disease populations, interventions, epidemiology or prediction of mortality. Searches used Web of Science, PubMed and Science Direct. Search terms included “cognitive frailty” OR ((“cognitive decline” OR “cognitive impairment”) AND (frail*)), with terms to elicit mechanisms, predictors, causes, pathways and risk factors. To ensure inclusion of animal and cell models, keywords such as “behavioural” or “cognitive decline” or “senescence”, were added. 206 papers were included. Descriptive analysis provided high-level categorisation of determinants from social and environmental through psychological to biological. Patterns distinguishing CF from Alzheimer’s disease were identified and social and psychological moderators and mediators of underlying biological and physiological changes and of trajectories of CF development were suggested as foci for further research.</p></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"101 ","pages":"Article 102461"},"PeriodicalIF":12.5,"publicationDate":"2024-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1568163724002794/pdfft?md5=0e1e3cbad26af2ec75c2e2cb1e91d951&pid=1-s2.0-S1568163724002794-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142238631","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}
Pub Date : 2024-09-14DOI: 10.1016/j.arr.2024.102504
Mahmood Akbar , Pranoy Toppo , Aamir Nazir
Recent research has illuminated the profound bidirectional communication between the gastrointestinal tract and the brain, furthering our understanding of neurological ailments facilitating possible therapeutic strategies. Technological advancements in high-throughput sequencing and multi-omics have unveiled significant alterations in gut microbiota and their metabolites in various neurological disorders. This review provides a thorough analysis of the role of microbiome-gut-brain axis in neurodegenerative disease pathology, linking it to reduced age-associated proteostasis. We discuss evidences that substantiate the existence of a gut-brain cross talk ranging from early clinical accounts of James Parkinson to Braak’s hypothesis. In addition to understanding of microbes, the review particularly entails specific metabolites which are altered in neurodegenerative diseases. The regulatory effects of microbial metabolites on protein clearance mechanisms, proposing their potential therapeutic implications, are also discussed. By integrating this information, we advocate for a combinatory therapeutic strategy that targets early intervention, aiming to restore proteostasis and ameliorate disease progression. This approach not only provides a new perspective on the pathogenesis of neurodegenerative diseases but also highlights innovative strategies to combat the increasing burden of these age-related disorders.
{"title":"Ageing, proteostasis, and the gut: Insights into neurological health and disease","authors":"Mahmood Akbar , Pranoy Toppo , Aamir Nazir","doi":"10.1016/j.arr.2024.102504","DOIUrl":"10.1016/j.arr.2024.102504","url":null,"abstract":"<div><p>Recent research has illuminated the profound bidirectional communication between the gastrointestinal tract and the brain, furthering our understanding of neurological ailments facilitating possible therapeutic strategies. Technological advancements in high-throughput sequencing and multi-omics have unveiled significant alterations in gut microbiota and their metabolites in various neurological disorders. This review provides a thorough analysis of the role of microbiome-gut-brain axis in neurodegenerative disease pathology, linking it to reduced age-associated proteostasis. We discuss evidences that substantiate the existence of a gut-brain cross talk ranging from early clinical accounts of James Parkinson to Braak’s hypothesis. In addition to understanding of microbes, the review particularly entails specific metabolites which are altered in neurodegenerative diseases. The regulatory effects of microbial metabolites on protein clearance mechanisms, proposing their potential therapeutic implications, are also discussed. By integrating this information, we advocate for a combinatory therapeutic strategy that targets early intervention, aiming to restore proteostasis and ameliorate disease progression. This approach not only provides a new perspective on the pathogenesis of neurodegenerative diseases but also highlights innovative strategies to combat the increasing burden of these age-related disorders.</p></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"101 ","pages":"Article 102504"},"PeriodicalIF":12.5,"publicationDate":"2024-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142272818","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}
Targeting senescent cells has recently emerged as a promising strategy for treating age-related diseases, such as atherosclerosis, which significantly contributes to global cardiovascular morbidity and mortality. This review elucidates the role of senescent cells in the development of atherosclerosis, including persistently damaging DNA, inducing oxidative stress and secreting pro-inflammatory factors known as the senescence-associated secretory phenotype. Therapeutic approaches targeting senescent cells to mitigate atherosclerosis are summarized in this review, which include the development of senotherapeutics and immunotherapies. These therapies are designed to either remove these cells or suppress their deleterious effects. These emerging therapies hold potential to decelerate or even alleviate the progression of AS, paving the way for new avenues in cardiovascular research and treatment.
{"title":"Targeting senescent cells in atherosclerosis: Pathways to novel therapies","authors":"Yuhan Tian , Sihang Shao , Haibo Feng , Rui Zeng , Shanshan Li , Qixiong Zhang","doi":"10.1016/j.arr.2024.102502","DOIUrl":"10.1016/j.arr.2024.102502","url":null,"abstract":"<div><p>Targeting senescent cells has recently emerged as a promising strategy for treating age-related diseases, such as atherosclerosis, which significantly contributes to global cardiovascular morbidity and mortality. This review elucidates the role of senescent cells in the development of atherosclerosis, including persistently damaging DNA, inducing oxidative stress and secreting pro-inflammatory factors known as the senescence-associated secretory phenotype. Therapeutic approaches targeting senescent cells to mitigate atherosclerosis are summarized in this review, which include the development of senotherapeutics and immunotherapies. These therapies are designed to either remove these cells or suppress their deleterious effects. These emerging therapies hold potential to decelerate or even alleviate the progression of AS, paving the way for new avenues in cardiovascular research and treatment.</p></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"101 ","pages":"Article 102502"},"PeriodicalIF":12.5,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142233038","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}
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