Aging brain最新文献

{"title":"Sleep deprivation aggravated amyloid β oligomers-induced damage to the cerebellum of rats: Evidence from magnetic resonance imaging","authors":"Wensheng Guo ,&nbsp;Xin Mao ,&nbsp;Ding Han ,&nbsp;Hongqi Wang ,&nbsp;Wanning Zhang ,&nbsp;Guitao Zhang ,&nbsp;Ning Zhang ,&nbsp;Binbin Nie ,&nbsp;Hui Li ,&nbsp;Yizhi Song ,&nbsp;Yan Wu ,&nbsp;Lirong Chang","doi":"10.1016/j.nbas.2023.100091","DOIUrl":"10.1016/j.nbas.2023.100091","url":null,"abstract":"<div><p>For quite a long time, researches on Alzheimer's disease (AD) primarily focused on the cortex and hippocampus, while the cerebellum has been ignored because of its abnormalities considered to appear in the late stage of AD. In recent years, increasing evidence suggest that the cerebellar pathological changes possibly occur in the preclinical phase of AD, which is also associated with sleep disorder. Sleep disturbance is a high risk factor of AD. However, the changes and roles of cerebellum has rarely been reported under conditions of AD accompanied with sleep disorders. In this study, using an amyloid-β oligomers (AβO)-induced rat model of AD subjected to sleep deprivation, combining with a 7.0 T animals structural magnetic resonance imaging (MRI), we assessed structural changes of cerebellum in MRI. Our results showed that sleep deprivation combined with AβO led to an increased FA value in the anterior lobe of cerebellum, decreased ADC value in the cerebellar lobes and cerebellar nuclei, and increased cerebellum volume. Besides that, sleep deprivation exacerbated the damage of AβO to the cerebellar structural network. This study demonstrated that sleep deprivation could aggravate the damage to cerebellum induced by AβO. The present findings provide supporting evidence for the involvement of cerebellum in the early pathology of AD and sleep loss. Our data would contribute to advancing the understanding of the mysterious role of cerebellum in AD and sleep disorders, as well as would be helpful for developing non-invasive MRI biomarkers for screening early AD patients with self-reported sleep disturbances.</p></div>","PeriodicalId":72131,"journal":{"name":"Aging brain","volume":"4 ","pages":"Article 100091"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/55/3b/main.PMC10432242.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10051620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling Parkinson’s risk factors","authors":"Sadashiva K. Pai","doi":"10.1016/j.nbas.2023.100073","DOIUrl":"10.1016/j.nbas.2023.100073","url":null,"abstract":"","PeriodicalId":72131,"journal":{"name":"Aging brain","volume":"3 ","pages":"Article 100073"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10112142/pdf/main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9740114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluating associations of RNFL thickness and multifocal VEP with cognitive assessment and brain MRI volumes in older adults: Optic nerve decline and cognitive change (ONDCC) initiative","authors":"Ting Shen ,&nbsp;Samran Sheriff ,&nbsp;Yuyi You ,&nbsp;Jiyang Jiang ,&nbsp;Angela Schulz ,&nbsp;Heather Francis ,&nbsp;Mehdi Mirzaei ,&nbsp;Danit Saks ,&nbsp;Nitin Chitranshi ,&nbsp;Veer Gupta ,&nbsp;Maria Fiatarone Singh ,&nbsp;Alexander Klistorner ,&nbsp;Wei Wen ,&nbsp;Perminder Sachdev ,&nbsp;Vivek K. Gupta ,&nbsp;Stuart L. Graham","doi":"10.1016/j.nbas.2022.100049","DOIUrl":"10.1016/j.nbas.2022.100049","url":null,"abstract":"<div><p>To examine the relationships of retinal structural (optical coherence tomography) and visual functional (multifocal visual evoked potentials, mfVEP) indices with neuropsychological and brain structural measurements in healthy older subjects. 95 participants (mean (SD) age 68.1 (9.0)) years were recruited in the Optic Nerve Decline and Cognitive Change (ONDCC) study in this observational clinical investigation. OCT was conducted for retinal nerve fibre layer (RNFL) and mfVEP for amplitude and latency measurements. Participants undertook neuropsychological tests for cognitive performance and MRI for volumetric evaluation of various brain regions. Generalised estimating equation models were used for association analysis (p &lt; 0.05). The brain volumetric measures including total grey matter (GM), cortex, thalamus, hippocampal and fourth ventricular volumes were significantly associated with global and sectoral RNFL. RNFL thickness correlated with delayed recalls of California verbal learning test (CVLT) and Rey complex figure test (RCFT). The mfVEP amplitudes associated with cerebral white matter (WM) and cingulate GM volumes in MRI and CVLT, RCFT and trail making test outcomes. A significant association of mfVEP latency with logical memory delayed recall and thalamus volume was also observed. Our results suggested significant association of specific RNFL and mfVEP measures with distinctive brain region volumes and cognitive tests reflecting performance in memory, visuospatial and executive functional domains. These findings indicate that the mfVEP and RNFL measurements may parallel brain structural and neuropsychological measures in the older population.</p></div>","PeriodicalId":72131,"journal":{"name":"Aging brain","volume":"2 ","pages":"Article 100049"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/15/94/main.PMC9997126.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9155244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring cortical proteins underlying the relation of neuroticism to cognitive resilience","authors":"Francine Grodstein ,&nbsp;Lei Yu ,&nbsp;Philip L. de Jager ,&nbsp;Allan Levey ,&nbsp;Nicholas T. Seyfried ,&nbsp;David A. Bennett","doi":"10.1016/j.nbas.2022.100031","DOIUrl":"10.1016/j.nbas.2022.100031","url":null,"abstract":"<div><p>Some individuals maintain cognitive health despite neuropathology. Targets impacting “cognitive resilience” may provide interventions for preventing dementia without decreasing neuropathology. Neuroticism represents the tendency to experience negative emotions, and is related to worse cognitive resilience. Exploring proteins associated with cognitive resilience risk factors, such as neuroticism, could yield new protein targets. We used 355 postmortem prefrontal cortex from two cohorts to measure 8356 proteins. We identified (i) proteins associated with both neuroticism and cognitive resilience, and (ii) proteins statistically mediating relations of neuroticism to cognitive resilience. We found two proteins, 40S ribosomal proteinS3 (RPS3) and branched chain keto acid dehydrogenase E1, subunit beta (BCKDHB), ranked in the top 1% of smallest p-values in parallel linear regression models of neuroticism to protein levels, and protein levels to cognitive decline resilience. In mediation models, RPS3 and BCKDHB accounted for 25% (p = 0.005) of the relation of neuroticism to cognitive resilience. Our sample size is modest, thus results may be due to chance (p-values did not meet Bonferroni significance) and will require further confirmation; however, investigating biologic mediators of associations of risk factors to cognitive resilience may help discover targets to promote cognitive resilience and reduce dementia.</p></div>","PeriodicalId":72131,"journal":{"name":"Aging brain","volume":"2 ","pages":"Article 100031"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/2d/5c/main.PMC9979250.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9394843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxytocin’s dynamic role across the lifespan","authors":"Kristin Audunsdottir ,&nbsp;Daniel S. Quintana","doi":"10.1016/j.nbas.2021.100028","DOIUrl":"10.1016/j.nbas.2021.100028","url":null,"abstract":"<div><p>Older adults have been neglected in biobehavioral oxytocin research. Emerging research indicates that oxytocin signaling activity fluctuates over the lifespan, which suggests that results from studies investigating youth and young adults cannot be easily generalized to older adults. The recruitment of a wider age range of research participants using a variety of research tools is required to uncover the role of the oxytocin signaling system over the lifespan and may reveal novel treatment target candidates in older adults, beyond social cognition and behavior.</p></div>","PeriodicalId":72131,"journal":{"name":"Aging brain","volume":"2 ","pages":"Article 100028"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9997153/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9095538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Future trends in brain aging research: Visuo-cognitive functions at stake during mobility and spatial navigation","authors":"Stephen Ramanoël ,&nbsp;Marion Durteste ,&nbsp;Alexandre Delaux ,&nbsp;Jean-Baptiste de Saint Aubert ,&nbsp;Angelo Arleo","doi":"10.1016/j.nbas.2022.100034","DOIUrl":"10.1016/j.nbas.2022.100034","url":null,"abstract":"<div><p>Aging leads to a complex pattern of structural and functional changes, gradually affecting sensorimotor, perceptual, and cognitive processes. These multiscale changes can hinder older adults’ interaction with their environment, progressively reducing their autonomy in performing tasks relevant to everyday life. Autonomy loss can further be aggravated by the onset and progression of neurodegenerative disorders (e.g., age-related macular degeneration at the sensory input level; and Alzheimer’s disease at the cognitive level). In this context, spatial cognition offers a representative case of high-level brain function that involves multimodal sensory processing, postural control, locomotion, spatial orientation, and wayfinding capabilities. Hence, studying spatial behavior and its neural bases can help identify early markers of pathogenic age-related processes. Until now, the neural correlates of spatial cognition have mostly been studied in static conditions thereby disregarding perceptual (other than visual) and motor aspects of natural navigation. In this review, we first demonstrate how visuo-motor integration and the allocation of cognitive resources during locomotion lie at the heart of real-world spatial navigation. Second, we present how technological advances such as immersive virtual reality and mobile neuroimaging solutions can enable researchers to explore the interplay between perception and action. Finally, we argue that the future of brain aging research in spatial navigation demands a widespread shift toward the use of naturalistic, ecologically valid experimental paradigms to address the challenges of mobility and autonomy decline across the lifespan.</p></div>","PeriodicalId":72131,"journal":{"name":"Aging brain","volume":"2 ","pages":"Article 100034"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/52/99/main.PMC9997160.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9469572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Apolipoprotein E loss of function: Influence on murine brain markers of physiology and pathology","authors":"Heather Buchanan ,&nbsp;Claire Hull ,&nbsp;Maria Cacho Barraza,&nbsp;Mirela Delibegovic,&nbsp;Bettina Platt","doi":"10.1016/j.nbas.2022.100055","DOIUrl":"10.1016/j.nbas.2022.100055","url":null,"abstract":"<div><p>The canonical role of Apolipoprotein E (ApoE) is related to lipid and cholesterol metabolism, however, additional functions of this protein have not been fully described. Given the association of ApoE with diseases such as Alzheimer’s Disease (AD), it is clear that further characterisation of its roles, especially within the brain, is needed.</p><p>Therefore, using protein and gene expression analyses of neonatal and 6-month old brain tissues from an ApoE knockout mouse model, we examined ApoE’s contribution to several CNS pathways, with an emphasis on those linked to AD. Early neonatal changes associated with ApoE−/− were observed, with decreased soluble phosphorylated tau (p-tau, –40 %), increased synaptophysin (+36 %) and microglial Iba1 protein levels (+25 %) vs controls. Progression of the phenotype was evident upon analysis of 6-month-old tissue, where decreased p-tau was also confirmed in the insoluble fraction, alongside reduced synaptic and increased amyloid precursor protein (APP) protein levels. An age comparison further underlined deviations from WT animals and thus the impact of ApoE loss on neuronal maturation.</p><p>Taken together, our data implicate ApoE modulation of multiple CNS roles. Loss of function is associated with alterations from birth, and include synaptic deficits, neuroinflammation, and changes to key AD pathologies, amyloid-β and tau.</p></div>","PeriodicalId":72131,"journal":{"name":"Aging brain","volume":"2 ","pages":"Article 100055"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/9c/bb/main.PMC9997145.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9469566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early memory deficits and extensive brain network disorganization in the AppNL-F/MAPT double knock-in mouse model of familial Alzheimer’s disease","authors":"Christopher Borcuk ,&nbsp;Céline Héraud ,&nbsp;Karine Herbeaux ,&nbsp;Margot Diringer ,&nbsp;Élodie Panzer ,&nbsp;Jil Scuto ,&nbsp;Shoko Hashimoto ,&nbsp;Takaomi C. Saido ,&nbsp;Takashi Saito ,&nbsp;Romain Goutagny ,&nbsp;Demian Battaglia ,&nbsp;Chantal Mathis","doi":"10.1016/j.nbas.2022.100042","DOIUrl":"10.1016/j.nbas.2022.100042","url":null,"abstract":"<div><p>A critical challenge in current research on Alzheimer’s disease (AD) is to clarify the relationship between network dysfunction and the emergence of subtle memory deficits in itspreclinical stage. The <em>AppNL-F/MAPT</em> double knock-in (dKI) model with humanized β-amyloid peptide (Aβ) and tau was used to investigate both memory and network dysfunctions at an early stage. Young male dKI mice (2 to 6 months) were tested in three tasks taxing different aspects of recognition memory affected in preclinical AD. An early deficit first appeared in the object-place association task at the age of 4 months, when increased levels of β-CTF and Aβ were detected in both the hippocampus and the medial temporal cortex, and tau pathology was found only in the medial temporal cortex. Object-place task-dependent c-Fos activation was then analyzed in 22 subregions across the medial prefrontal cortex, claustrum, retrosplenial cortex, and medial temporal lobe. Increased c-Fos activation was detected in the entorhinal cortex and the claustrum of dKI mice. During recall, network efficiency was reduced across cingulate regions with a major disruption of information flow through the retrosplenial cortex. Our findings suggest that early perirhinal-entorhinal pathology is associated with abnormal activity which may spread to downstream regions such as the claustrum, the medial prefrontal cortex and ultimately the key retrosplenial hub which relays information from frontal to temporal lobes. The similarity between our findings and those reported in preclinical stages of AD suggests that the <em>AppNL-F/MAPT</em> dKI model has a high potential for providing key insights into preclinical AD.</p></div>","PeriodicalId":72131,"journal":{"name":"Aging brain","volume":"2 ","pages":"Article 100042"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/10/e4/main.PMC9997176.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9099901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Asymmetric amyloid deposition in preclinical Alzheimer’s disease: A PET study","authors":"Pernille L. Kjeldsen ,&nbsp;Peter Parbo ,&nbsp;Kim V. Hansen ,&nbsp;Joel F.A. Aanerud ,&nbsp;Rola Ismail ,&nbsp;Peter H. Nissen ,&nbsp;Rikke B. Dalby ,&nbsp;Malene F. Damholdt ,&nbsp;Per Borghammer ,&nbsp;David J. Brooks","doi":"10.1016/j.nbas.2022.100048","DOIUrl":"10.1016/j.nbas.2022.100048","url":null,"abstract":"<div><h3>Introduction</h3><p>The typical spatial pattern of amyloid-β (Aβ) in diagnosed Alzheimer’s disease (AD) is that of a symmetrical hemispheric distribution. However, Aβ may be asymmetrically distributed in early stages of AD. Aβ distribution on PET has previously been explored in MCI and AD, but it has yet to be directly investigated in preclinical AD (pAD). We examined how Aβ was distributed in individuals with pAD and MCI using ¹¹C-Pittsburgh Compound B (PiB) PET.</p></div><div><h3>Methods</h3><p>In this PET study, 79 subjects were retrospectively enrolled, including 34 controls, 24 pAD, and 21 MCI. All subjects underwent <em>APOE</em> genotyping, ¹¹C-PiB PET, MRI, and cognitive testing. We explored differences in Aβ load, Aβ lateralisation, and Aβ distribution, as well as associations between Aβ distribution and cognition.</p></div><div><h3>Results</h3><p>The Aβ asymmetry index (AI) differed between groups, with pAD having the highest Aβ AI as compared to both controls and MCI. There was no clear Aβ lateralisation in pAD, but there was a non-significant trend towards Aβ being more left-lateralised in MCI. There were no correlations between the cognitive scores and Aβ AI or Aβ lateralisation in pAD or MCI.</p></div><div><h3>Conclusion</h3><p>The distribution of Aβ is most asymmetrical in pAD, as Aβ first starts accumulating, and it then becomes less asymmetrical in MCI, when Aβ has spread further, suggesting that more pronounced asymmetrical Aβ distribution may be a distinguishing factor in pAD. Longitudinal studies examining the distribution of Aβ across the AD continuum are needed.</p></div>","PeriodicalId":72131,"journal":{"name":"Aging brain","volume":"2 ","pages":"Article 100048"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/56/bf/main.PMC9997142.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9155242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sleep, Sirtuin 1 and Alzheimer’s disease: A review","authors":"Mehrane Mehramiz ,&nbsp;Tenielle Porter ,&nbsp;Simon M. Laws ,&nbsp;Stephanie R. Rainey-Smith","doi":"10.1016/j.nbas.2022.100050","DOIUrl":"10.1016/j.nbas.2022.100050","url":null,"abstract":"<div><p>Sleep plays a major role in brain health, and cognition. Disrupted sleep is a well-described symptom of Alzheimer’s disease (AD). However, accumulating evidence suggests suboptimal sleep also increases AD risk. The deacetylase Sirtuin 1 (Sirt 1), encoded by the <em>SIRT1</em> gene, impacts sleep via its relationship to wake-sleep neurotransmitters and somnogens. Evidence from animal and human studies supports a significant and complex relationship between sleep, Sirt 1/ <em>SIRT1</em> and AD. Numerous hypotheses attempt to explain the critical impact of Sirt 1/ <em>SIRT1</em> on wake- and sleep- promoting neurons, their related mechanisms and neurotransmitters. However, there is a paucity of studies assessing the interaction between sleep and Sirt 1/ <em>SIRT1</em>, as a principal component of sleep regulation, on AD pathology. In this review, we explore the potential association between Sirt 1/ <em>SIRT1</em>, sleep, and AD aetiology. Given sleep is a likely modifiable risk factor for AD, and recent studies suggest Sirt 1/ <em>SIRT1</em> activation can be modulated by lifestyle or dietary approaches, further research in this area is required to explore its potential as a target for AD prevention and treatment.</p></div>","PeriodicalId":72131,"journal":{"name":"Aging brain","volume":"2 ","pages":"Article 100050"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/4d/f6/main.PMC9997138.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9453772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}