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Calcineurin/NFAT inhibitors maintain cognition in a preclinical prevention study in an aging canine model of Alzheimer disease 钙神经蛋白/NFAT抑制剂可在老年痴呆症犬模型的临床前预防研究中维持认知能力。
IF 3.7 3区 医学 Q2 GERIATRICS & GERONTOLOGY Pub Date : 2024-11-10 DOI: 10.1016/j.neurobiolaging.2024.11.003
Lorena Sordo , Margo F. Ubele , Kathy A. Boaz , Jennifer L. Mefford , Erin Dehnart Jones , Katie L. McCarty , Hollie Y. van Rooyen , Jeffrey Smiley , Stasia A. Bembenek Bailey , Jessica A. Perpich , Beverly Meacham , David K. Powell , Frederick Bresch , Jacob W. Crump , Michael J. Phelan , Jessica A. Noche , Craig E. Stark , László G. Puskás , Christopher M. Norris , Elizabeth Head
Brain signaling of calcineurin (CN) and nuclear factor of activated T-cells (NFAT) transcription factor increases in Alzheimer disease (AD) and is associated with synaptic loss, neurodegeneration, neuroinflammation, amyloid-β (Aβ) production, and cognitive decline. CN/NFAT inhibitors ameliorate these neuropathologies in mouse models of AD. Further, chronic use of tacrolimus in transplant patients reduces risk of AD. Beagles naturally develop Aβ plaques and cognitive dysfunction. We evaluated the impact of FDA-approved CN inhibitor, tacrolimus, and experimental NFAT inhibitor, Q134R, on cognitive outcomes during a three-year prevention study in 37 middle-aged beagles. While beagles treated with CN/NFAT inhibitors showed differences in the pattern of cognitive maintenance and duration of their effect, there was improvement in spatial learning, as well as maintenance of memory, attention, and working memory relative to placebo dogs. CN/NFAT inhibition is a promising target for prevention of cognitive decline that may be rapidly implemented in human clinical trials.
在阿尔茨海默病(AD)中,脑内钙神经蛋白(CN)和活化T细胞核因子(NFAT)转录因子的信号增强,并与突触丢失、神经变性、神经炎症、淀粉样蛋白-β(Aβ)生成和认知能力下降有关。CN/NFAT抑制剂可改善AD小鼠模型中的这些神经病理变化。此外,移植患者长期使用他克莫司可降低罹患注意力缺失症的风险。比格犬会自然形成 Aβ 斑块和认知功能障碍。我们评估了美国 FDA 批准的 CN 抑制剂他克莫司和实验性 NFAT 抑制剂 Q134R 对 37 只中年比格犬在为期三年的预防研究中认知结果的影响。虽然接受 CN/NFAT 抑制剂治疗的猎犬在认知能力维持模式和效果持续时间上存在差异,但与安慰剂犬相比,它们的空间学习能力以及记忆力、注意力和工作记忆的维持能力都有所改善。CN/NFAT抑制剂是一种很有前景的预防认知能力下降的靶点,可迅速用于人类临床试验。
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引用次数: 0
Hypertension may associate with cerebral small vessel disease and infarcts through the pathway of intracranial atherosclerosis 高血压可能会通过颅内动脉粥样硬化的途径导致脑小血管疾病和脑梗塞。
IF 3.7 3区 医学 Q2 GERIATRICS & GERONTOLOGY Pub Date : 2024-11-07 DOI: 10.1016/j.neurobiolaging.2024.11.001
Marcelo Kenzo Naya Takahashi , Regina Silva Paradela , Lea Tenenholz Grinberg , Renata Elaine Paraizo Leite , Daniela Souza Farias-Itao , Vitor Ribeiro Paes , Maria Eduarda Braga , Michel Satya Naslavsky , Mayana Zatz , Wilson Jacob-Filho , Ricardo Nitrini , Carlos Augusto Pasqualucci , Claudia Kimie Suemoto
Hypertension, a major modifiable risk factor for cardiovascular diseases, is linked to late-life neurocognitive disorders such as vascular dementia and Alzheimer's disease (AD). This study explores the associations between hypertension, intracranial atherosclerotic disease (ICAD), cerebral small vessel disease (cSVD), and Alzheimer's disease neuropathologic change (ADNC) in a large community-based autopsy study.
This cross-sectional study used data from the Biobank for Aging Studies of the University of São Paulo Medical School. Sociodemographic and clinical information was gathered from a reliable next-of-kin informant. Neurofibrillary tangles, neuritic plaques, lacunar infarcts, hyaline arteriolosclerosis, and cerebral amyloid angiopathy were evaluated. Causal mediation analyses with natural effect models were performed to examine indirect associations of hypertension with cerebrovascular pathologies and ADNC through morphometric measurements of intracranial artery lumen obstruction.
Hypertensive participants (n = 354) presented a higher rate of stenosed arteries (obstruction ≥ 50 %), critically stenosed arteries (obstruction ≥ 70 %), and more severe ICAD, shown by higher maximum and mean obstruction indexes compared to nonhypertensive participants (n = 166). These measurements of atherosclerosis were associated with neurofibrillary tangles and cSVD lesions. Hypertension was indirectly associated with hyaline arteriolosclerosis and lacunar infarcts through the pathway of ICAD. Presenting hypertension indirectly increased the odds of displaying hyaline arteriolosclerosis by 26 % (95 % CI: 1.08, 1.45, p = 0.002) and lacunar infarcts by 17 % (95 % CI: 1.01, 1.35, p = 0.029). Cognitive and APOE ε4 carrier status did not alter the investigated associations. In this community sample, hypertension was indirectly associated with cSVD through ICAD.
高血压是心血管疾病的主要可改变风险因素,它与血管性痴呆和阿尔茨海默病(AD)等晚年神经认知障碍有关。本研究在一项大型社区尸检研究中探讨了高血压、颅内动脉粥样硬化性疾病(ICAD)、脑小血管疾病(cSVD)和阿尔茨海默病神经病理变化(ADNC)之间的关联。这项横断面研究使用了圣保罗大学医学院老龄化研究生物库的数据。社会人口学和临床信息是从可靠的近亲信息提供者处收集的。对神经纤维缠结、神经斑块、腔隙性脑梗塞、透明动脉硬化和脑淀粉样血管病进行了评估。利用自然效应模型进行因果中介分析,通过颅内动脉管腔阻塞的形态测量,研究高血压与脑血管病变和ADNC的间接关系。与非高血压参试者(n = 166)相比,高血压参试者(n = 354)的动脉狭窄率(阻塞率≥ 50%)、严重狭窄率(阻塞率≥ 70%)和 ICAD 严重程度更高,表现为最大阻塞指数和平均阻塞指数更高。这些动脉粥样硬化的测量结果与神经纤维缠结和cSVD病变有关。高血压通过 ICAD 途径与透明动脉硬化和腔隙性梗死间接相关。出现高血压会间接增加透明动脉硬化的几率26%(95% CI:1.08, 1.45, p = 0.002)和腔隙性脑梗塞的几率17%(95% CI:1.01, 1.35, p = 0.029)。认知能力和 APOE ε4 携带者状况并没有改变所调查的关联。在这一社区样本中,高血压通过 ICAD 与心血管疾病间接相关。
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引用次数: 0
A neural implementation of cognitive reserve: Insights from a longitudinal fMRI study of set-switching in aging 认知储备的神经实现:对衰老过程中集合切换的纵向 fMRI 研究的启示
IF 3.7 3区 医学 Q2 GERIATRICS & GERONTOLOGY Pub Date : 2024-10-31 DOI: 10.1016/j.neurobiolaging.2024.10.008
Fatemeh Hasanzadeh , Christian Habeck , Yunglin Gazes , Yaakov Stern
Aging is often accompanied by changes in brain structure and executive functions, particularly in tasks involving cognitive flexibility, such as task-switching. However, substantial individual differences in the degree of cognitive impairment indicate that some individuals can cope with brain changes more effectively than others, suggesting higher cognitive reserve (CR). This study identified a neural basis for CR by examining the longitudinal relationship between task-related brain activation, structural brain changes, and changes in cognitive performance during an executive task-switching paradigm including single and dual conditions. Fifty-two older individuals were assessed at baseline and followed up after five years. Structural brain changes related to task-switching performance were analyzed using elastic net regression. Task-related functional brain activation was measured using ordinal trends canonical variate analysis (OrT CVA), capturing patterns of activation increasing from single to dual conditions. A differential task-related expression score (dOrT) was calculated as the difference in pattern expression scores between single and dual conditions at baseline. A linear regression model tested whether dOrT moderated the impact of brain changes on changes in switch cost over five years. Results showed a significant interaction between changes in brain structure and dOrT activation on switch cost change, indicating a moderation effect of task-related activation. Higher dOrT buffered the impact of brain structural decline on switch costs, enabling older adults to better cope with age-related brain structural changes and preserve cognitive flexibility. These findings suggest that these task-related activation patterns represent a neural basis for CR.
衰老往往伴随着大脑结构和执行功能的变化,特别是在涉及认知灵活性的任务中,如任务转换。然而,认知障碍程度的巨大个体差异表明,有些人比其他人能更有效地应对大脑的变化,这表明他们具有较高的认知储备(CR)。本研究通过研究任务相关的大脑激活、大脑结构变化以及在执行任务切换范式(包括单一和双重条件)中认知表现的变化之间的纵向关系,确定了认知储备的神经基础。52名老年人接受了基线评估和五年后的随访。使用弹性网回归分析了与任务切换表现相关的大脑结构变化。与任务相关的大脑功能激活采用顺序趋势典型变异分析(OrT CVA)进行测量,捕捉从单一条件到双重条件的激活增加模式。与任务相关的差异表达得分(dOrT)被计算为基线时单一和双重条件下模式表达得分的差异。线性回归模型测试了 dOrT 是否会调节大脑变化对五年内转换成本变化的影响。结果显示,大脑结构变化和 dOrT 激活对转换成本变化的影响存在明显的交互作用,这表明任务相关激活具有调节作用。较高的dOrT可以缓冲大脑结构衰退对转换成本的影响,使老年人能够更好地应对与年龄相关的大脑结构变化,保持认知灵活性。这些发现表明,这些与任务相关的激活模式代表了 CR 的神经基础。
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引用次数: 0
M1 muscarinic receptor activation reverses age-related memory updating impairment in mice 激活 M1 肌激酶受体可逆转小鼠与年龄相关的记忆更新损伤。
IF 3.7 3区 医学 Q2 GERIATRICS & GERONTOLOGY Pub Date : 2024-10-28 DOI: 10.1016/j.neurobiolaging.2024.10.007
Kristen H. Jardine , Emily P. Minard , Cassidy E. Wideman , Haley Edwards , Karim H. Abouelnaga , William S. Messer , Boyer D. Winters
Previously consolidated memories can become temporarily labile upon reactivation. Reactivation-based memory updating is chiefly studied in young subjects, so we aimed to assess this process across the lifespan. To do this, we developed a behavioural paradigm wherein a reactivated object memory is updated with contextual information; 3-month-old and 6-month-old male C57BL/6 mice displayed object memory updating, but 12-month-old mice did not. We found that M1 muscarinic acetylcholine receptor signaling during reactivation was necessary for object memory updating in the young mice. Next, we targeted this mechanism in an attempt to facilitate object memory updating in aging mice. Remarkably, systemic pharmacological M1 receptor activation reversed the age-related deficit. Quantification of cholinergic system markers within perirhinal cortex revealed subtle cellular changes that may contribute to differential performance across age groups. These findings suggest that natural cholinergic change across the lifespan contributes to inflexible memory in the aging brain.
先前巩固的记忆在重新激活时会变得暂时不稳定。基于再激活的记忆更新主要是在年轻受试者身上进行研究的,因此我们的目标是评估整个生命周期的这一过程。为此,我们开发了一种行为范式,用上下文信息更新重新激活的物体记忆;3 个月大和 6 个月大的雄性 C57BL/6 小鼠显示出物体记忆更新,而 12 个月大的小鼠则没有。我们发现,在重新激活过程中,M1毒蕈碱乙酰胆碱受体信号对于幼鼠的物体记忆更新是必要的。接下来,我们针对这一机制尝试促进衰老小鼠的物体记忆更新。值得注意的是,全身药理激活 M1 受体可以逆转与年龄相关的记忆缺失。对脑周皮层内胆碱能系统标记物的定量分析发现了微妙的细胞变化,这些变化可能是造成不同年龄组小鼠表现差异的原因。这些研究结果表明,胆碱能在整个生命周期中的自然变化是导致老龄大脑记忆不灵活的原因之一。
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引用次数: 0
Exploring the links among brain iron accumulation, cognitive performance, and dietary intake in older adults: A longitudinal MRI study 探索老年人脑铁积累、认知能力和饮食摄入之间的联系:磁共振成像纵向研究
IF 3.7 3区 医学 Q2 GERIATRICS & GERONTOLOGY Pub Date : 2024-10-19 DOI: 10.1016/j.neurobiolaging.2024.10.006
Valentinos Zachariou , Colleen Pappas , Christopher E. Bauer , Elayna R. Seago , Brian T. Gold
This study evaluated longitudinal brain iron accumulation in older adults, its association with cognition, and the role of specific nutrients in mitigating iron accumulation. MRI-based, quantitative susceptibility mapping estimates of brain iron concentration were acquired from seventy-two healthy older adults (47 women, ages 60–86) at a baseline timepoint (TP1) and a follow-up timepoint (TP2) 2.5–3.0 years later. Dietary intake was evaluated at baseline using a validated questionnaire. Cognitive performance was assessed at TP2 using the uniform data set (Version 3) neuropsychological tests of episodic memory (MEM) and executive function (EF). Voxel-wise, linear mixed-effects models, adjusted for longitudinal gray matter volume alterations, age, and several non-dietary lifestyle factors revealed brain iron accumulation in multiple subcortical and cortical brain regions, which was negatively associated with both MEM and EF performance at T2. However, consumption of specific dietary nutrients at TP1 was associated with reduced brain iron accumulation. Our study provides a map of brain regions showing iron accumulation in older adults over a short 2.5-year follow-up and indicates that certain dietary nutrients may slow brain iron accumulation.
这项研究评估了老年人大脑铁的纵向积累、其与认知能力的关系以及特定营养素在减轻铁积累方面的作用。在基线时间点(TP1)和 2.5-3.0 年后的随访时间点(TP2),对 72 名健康老年人(47 名女性,年龄在 60-86 岁之间)进行了基于磁共振成像的脑铁浓度定量易感图评估。在基线时间点使用有效问卷对饮食摄入量进行评估。在 TP2 阶段,采用统一数据集(第 3 版)神经心理学测试对认知能力进行评估,测试内容包括外显记忆 (MEM) 和执行功能 (EF)。经纵向灰质体积变化、年龄和几种非膳食生活方式因素调整的体素线性混合效应模型显示,大脑皮质下和皮质多个区域的脑铁积累与 T2 阶段的 MEM 和 EF 表现呈负相关。然而,在TP1阶段摄入特定的膳食营养素与脑铁积累的减少有关。我们的研究提供了一幅在短短2.5年随访期间显示老年人铁积累的大脑区域图,并表明某些膳食营养素可能会减缓大脑铁的积累。
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引用次数: 0
Amyloid pathology and cognitive impairment in hAβ-KI and APPSAA-KI mouse models of Alzheimer's disease hAβ-KI 和 APPSAA-KI 阿尔茨海默病小鼠模型中的淀粉样病理和认知障碍。
IF 3.7 3区 医学 Q2 GERIATRICS & GERONTOLOGY Pub Date : 2024-10-19 DOI: 10.1016/j.neurobiolaging.2024.10.005
Wenyan Lu, Francis Shue, Aishe Kurti, Suren Jeevaratnam, Jesse R. Macyczko, Bhaskar Roy, Taha Izhar, Ni Wang, Guojun Bu , Takahisa Kanekiyo, Yonghe Li
The hAβ-KI and APPSAA-KI are two amyloid models that harbor mutations in the endogenous mouse App gene. Both hAβ-KI and APPSAA-KI mice contain a humanized Aβ sequence, and APPSAA-KI mice carry three additional familial AD mutations. We herein report that the Aβ levels and Aβ42/Aβ40 ratio in APPSAA-KI homozygotes are dramatically higher than those in hAβ-KI homozygotes at 14 months of age. In addition, APPSAA-KI mice display a widespread distribution of amyloid plaques in the brain, whereas the plaques are undetectable in hAβ-KI mice. Moreover, there are no sex differences in amyloid pathology in APPSAA-KI mice. Both APPSAA-KI and hAβ-KI mice exhibit cognitive impairments, wherein no significant differences are found between these two models, although APPSAA KI mice show a trend towards worse cognitive function. Notably, female hAβ-KI and APPSAA-KI mice have a more pronounced cognitive impairments compared to their respective males. Our findings suggest that Aβ humanization contributes to cognitive deficits in APPSAA-KI mice, and that amyloid deposition might not be closely associated with cognitive impairments in APPSAA-KI mice.
hAβ-KI和APPSAA-KI是两种携带内源性小鼠App基因突变的淀粉样蛋白模型。hAβ-KI和APPSAA-KI小鼠都含有人源化的Aβ序列,APPSAA-KI小鼠还携带三个家族性AD突变。我们在此报告,14 个月大时,APPSAA-KI 基因同源小鼠的 Aβ 水平和 Aβ42/Aβ40 比率显著高于 hAβ-KI 基因同源小鼠。此外,APPSAA-KI 小鼠的大脑中广泛分布着淀粉样蛋白斑块,而 hAβ-KI 小鼠则检测不到这些斑块。此外,APPSAA-KI 小鼠的淀粉样蛋白病理变化没有性别差异。APPSAA-KI 小鼠和 hAβ-KI 小鼠都表现出认知功能障碍,尽管 APPSAA KI 小鼠的认知功能有变差的趋势,但这两种模型之间没有发现明显的差异。值得注意的是,与雄性小鼠相比,雌性 hAβ-KI 和 APPSAA-KI 小鼠的认知功能障碍更为明显。我们的研究结果表明,Aβ人源化是导致APPSAA-KI小鼠认知障碍的原因之一,而淀粉样蛋白沉积可能与APPSAA-KI小鼠的认知障碍并无密切联系。
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引用次数: 0
Longitudinal relationships between Aβ and tau to executive function and memory in cognitively normal older adults 认知正常老年人的 Aβ 和 tau 与执行功能和记忆的纵向关系
IF 3.7 3区 医学 Q2 GERIATRICS & GERONTOLOGY Pub Date : 2024-10-19 DOI: 10.1016/j.neurobiolaging.2024.10.004
Xi Chen , Alexis Juarez , Suzanne Mason , Sarah Kobayashi , Suzanne L. Baker , Theresa M. Harrison , Susan M. Landau , William J. Jagust
The early accumulation of AD pathology such as Aβ and tau in cognitively normal older people is predictive of cognitive decline, but it has been difficult to dissociate the cognitive effects of these two proteins. Early Aβ and tau target distinct brain regions that have different functional roles. Here, we assessed specific longitudinal pathology-cognition associations in seventy-six cognitively normal older adults from the Berkeley Aging Cohort Study who underwent longitudinal PiB PET, FTP PET, and cognitive assessments. Using linear mixed-effects models to estimate longitudinal changes and residual approach to characterizing cognitive domain-specific associations, we found that Aβ accumulation, especially in frontal/parietal regions, was associated with faster decline in executive function, not memory, whereas tau accumulation, especially in left entorhinal/parahippocampal regions, was associated with faster decline in memory, not executive function, supporting an “Aβ-executive function, tau-memory” double-dissociation in cognitively normal older people. These specific relationships between accumulating pathology and domain-specific cognitive decline may be due to the particular vulnerabilities of the frontal-parietal executive network to Aβ and temporal memory network to tau.
在认知能力正常的老年人中,Aβ和tau等AD病理蛋白的早期积累可预测认知能力的下降,但这两种蛋白对认知能力的影响一直难以区分。早期的Aβ和tau针对不同的大脑区域,具有不同的功能作用。在此,我们对伯克利老龄队列研究(Berkeley Aging Cohort Study)中76名认知正常的老年人进行了纵向PiB PET、FTP PET和认知评估,评估了特定的纵向病理-认知关联。我们使用线性混合效应模型来估计纵向变化,并使用残差法来描述认知领域的特异性关联,结果发现,Aβ的积累(尤其是在额叶/顶叶区域)与执行功能(而非记忆)的快速衰退有关,而tau的积累(尤其是在左侧内侧/副海马区域)与记忆(而非执行功能)的快速衰退有关,这支持了认知正常老年人的 "Aβ-执行功能,tau-记忆 "双重关联。病理累积与特定领域认知能力下降之间的这些特殊关系可能是由于额叶-顶叶执行网络对Aβ和颞叶记忆网络对tau的特殊脆弱性。
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引用次数: 0
Editorial Advisory Board 编辑顾问委员会
IF 3.7 3区 医学 Q2 GERIATRICS & GERONTOLOGY Pub Date : 2024-10-18 DOI: 10.1016/S0197-4580(24)00176-3
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引用次数: 0
Hearing loss and its relation to longitudinal changes in white matter microstructure in older adults: The Rotterdam Study 听力损失及其与老年人白质微结构纵向变化的关系:鹿特丹研究
IF 3.7 3区 医学 Q2 GERIATRICS & GERONTOLOGY Pub Date : 2024-10-18 DOI: 10.1016/j.neurobiolaging.2024.10.003
Jordi H.C. Boons , Elisabeth J. Vinke , Gertjan Dingemanse , Bernd Kremer , André Goedegebure , Meike W. Vernooij
Hearing loss is considered a potentially modifiable risk factor for dementia. The sensory deprivation theory postulates that hearing loss adversely affects cognition in older adults through structural brain changes, but longitudinal studies are scarce. To find evidence for a possible detrimental effect of hearing loss on white matter microstructure, we carried out a longitudinal study in the population-based Rotterdam Study. A total of 1877 participants with a median age at baseline of 56.4 years (IQR: [52.2–60.0]) underwent audiometry and had longitudinal diffusion imaging data available with a mean follow-up of 4.0 years. A lower level of hearing acuity was associated with worse white matter microstructure in the left uncinate fasciculus and superior longitudinal fasciculus at baseline. Poorer hearing acuity was also associated with faster microstructural deterioration over time in the left superior longitudinal fasciculus. The strongest effects were observed for low-frequency hearing thresholds, while the high-frequency thresholds showed the weakest associations. These results suggest that hearing loss may contribute to the age-related decline in brain structure, consistent with the sensory deprivation theory.
听力损失被认为是痴呆症的潜在风险因素。感觉剥夺理论推测,听力损失会通过大脑结构变化对老年人的认知能力产生不利影响,但纵向研究却很少。为了寻找听力损失可能对白质微结构产生不利影响的证据,我们在基于人群的鹿特丹研究中开展了一项纵向研究。共有 1877 名基线年龄中位数为 56.4 岁(IQR:[52.2-60.0])的参与者接受了听力测定,并获得了纵向扩散成像数据,平均随访时间为 4.0 年。听力敏锐度较低与基线时左侧钩状筋膜和上纵筋膜的白质微结构较差有关。随着时间的推移,听力敏锐度越低,左上纵筋膜的微结构退化越快。低频听阈的影响最强,而高频听阈的影响最弱。这些结果表明,听力损失可能会导致与年龄相关的大脑结构衰退,这与感觉剥夺理论是一致的。
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引用次数: 0
Alcohol consumption confers lasting impacts on prefrontal cortical neuron intrinsic excitability and spontaneous neurotransmitter signaling in the aging brain in mice 饮酒对小鼠衰老大脑前额叶皮质神经元固有兴奋性和自发神经递质信号转导产生持久影响。
IF 3.7 3区 医学 Q2 GERIATRICS & GERONTOLOGY Pub Date : 2024-10-15 DOI: 10.1016/j.neurobiolaging.2024.09.014
Grace C. Smith , Keith R. Griffith , Avery R. Sicher , Dakota F. Brockway , Elizabeth A. Proctor , Nicole A. Crowley
Both alcohol use disorder (AUD) and cognitive decline include disruption in the balance of excitation and inhibition in the cortex, but the potential role of alcohol use on excitation and inhibition on the aging brain is unclear. We examined the effect of moderate voluntary binge alcohol consumption on the aged, pre-disease neuronal environment by measuring intrinsic excitability and spontaneous neurotransmission on prefrontal cortical pyramidal (excitatory, glutamatergic) and non-pyramidal (inhibitory, GABAergic) neurons following a prolonged period of abstinence from alcohol in mice. Results highlight that binge alcohol consumption has lasting impacts on the electrophysiological properties of prefrontal cortical neurons. A profound increase in excitatory events onto layer 2/3 non-pyramidal neurons following alcohol consumption was seen, along with altered intrinsic excitability of pyramidal neurons, which could have a range of effects on cognitive disorder progression, such as Alzheimer’s Disease, in humans. These results indicate that moderate voluntary alcohol influences the pre-disease environment in aging and highlight the need for further mechanistic investigation into this risk factor.
酒精使用障碍(AUD)和认知能力下降都包括大脑皮层兴奋和抑制平衡的破坏,但酒精使用对老化大脑兴奋和抑制的潜在作用尚不清楚。我们通过测量小鼠长期戒酒后前额叶皮层锥体(兴奋性,谷氨酸能)和非锥体(抑制性,GABA能)神经元的内在兴奋性和自发神经传递,研究了中度自愿暴饮对老化、病前神经元环境的影响。研究结果表明,酗酒会对前额叶皮质神经元的电生理特性产生持久影响。饮酒后,第 2/3 层非锥体神经元的兴奋事件显著增加,锥体神经元的固有兴奋性也发生了改变,这可能会对人类认知障碍(如阿尔茨海默病)的发展产生一系列影响。这些结果表明,适度自愿饮酒会影响衰老过程中的病前环境,并强调了对这一风险因素进行进一步机理研究的必要性。
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引用次数: 0
期刊
Neurobiology of Aging
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