IF 2.7 Q3 CLINICAL NEUROLOGY

Aging brain

Pub Date : 2025-12-12 DOI: 10.1016/j.nbas.2025.100155

Kimberly Albert , Brian Boyd , Brenna McDonald , Julie Dumas , Andrew Saykin , Warren Taylor , Paul Newhouse

Subjective Cognitive Decline (SCD) is the perception of a persistent decline in cognitive function and self-reported concerns over cognitive ability in older adults with normal objective cognitive performance. SCD is associated with increased Alzheimer’s Disease (AD) risk and early AD pathology. The neurobiological underpinnings of SCD and cognitive or neural circuit alterations during SCD remain unclear. This study aimed to identify patterns of brain network functional connectivity that are associated with quantitative measures of cognitive concerns, and to examine how these functional patterns are related to performance in the cognitive domains of visual-spatial processing, attentional control, and working memory. This analysis combined data from three studies of cognitively healthy older adults which included a quantified assessment of cognitive concern severity, resting-state fMRI, and cognitive testing in the above domains. We examined brain network-to-network functional connectivity associated with self-rated cognitive concern severity, and then how the identified patterns relate to cognitive performance. Results showed that greater cognitive concern severity was associated with unique patterns of functional connectivity between the Default Mode Network and the Language and Salience Networks in older adults without objective cognitive impairment. While greater cognitive concern severity alone was associated with slower processing reaction time, these functional connectivity patterns were associated with faster processing reaction time. This suggests that these functional connectivity patterns may alter the relationship between cognitive concern severity and psychomotor slowing. These findings support that despite the perception of cognitive changes in older adults, normal cognitive performance may be maintained through functional connectivity changes in brain networks important to directing visual-spatial attention and processing.

主观认知衰退（SCD）是指客观认知能力正常的老年人认知功能持续下降和自我报告的认知能力问题。SCD与阿尔茨海默病（AD）风险增加和早期AD病理相关。SCD的神经生物学基础以及SCD期间的认知或神经回路改变尚不清楚。本研究旨在确定与认知关注的定量测量相关的大脑网络功能连接模式，并研究这些功能模式如何与视觉空间处理、注意力控制和工作记忆的认知领域的表现相关。该分析结合了三项对认知健康老年人的研究数据，包括对认知担忧严重程度的量化评估、静息状态fMRI和上述领域的认知测试。我们研究了与自我评估的认知关注严重程度相关的大脑网络对网络功能连接，然后研究了识别的模式与认知表现的关系。结果表明，在没有客观认知障碍的老年人中，更大的认知关注严重程度与默认模式网络与语言和显著性网络之间的独特功能连接模式有关。而更大的认知关注严重性与更慢的处理反应时间有关，这些功能连接模式与更快的处理反应时间有关。这表明这些功能连接模式可能会改变认知关注严重程度和精神运动减缓之间的关系。这些发现表明，尽管老年人的认知能力发生了变化，但正常的认知表现可能是通过大脑网络的功能连接变化来维持的，这些网络对指导视觉空间注意力和处理很重要。

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引用次数: 0

Lipofuscin autofluorescence confounds intracellular amyloid β detection in the aged mouse brain. 脂褐素自身荧光混淆了老年小鼠大脑中细胞内淀粉样蛋白β的检测。

IF 2.7 Q3 CLINICAL NEUROLOGY

Aging brain

Pub Date : 2025-08-08 eCollection Date: 2025-01-01 DOI: 10.1016/j.nbas.2025.100148

Godfried Dougnon, Hideaki Matsui

Intracellular amyloid β (Aβ) accumulation is a contentious feature of Alzheimer's disease (AD), increasingly reported in young adults and aged animal models of AD. However, autofluorescent lipofuscin granules which consist of a mixture of highly oxidized lipids, misfolded proteins, and metals, accumulates with aging in neurons and microglia and renders difficult the interpretation of immunofluorescence-based studies. Here, we show that lipofuscin accumulation in aged wild-type (WT) mouse brains exhibits significant spectral overlap with commonly used antibodies for Aβ detection, leading to potential misinterpretation of intracellular Aβ signals. Through a combination of dye staining, immunohistochemistry (IHC), and confocal microscopy, we show that fluorescence signals resembling intracellular Aβ and commonly reported in aged animal models of AD, may reflect the presence of lipofuscin granules. Importantly, these signals persisted in control sections where primary Aβ antibodies were omitted, but disappeared following TrueBlack autofluorescence quencher. We also performed Aβ immunofluorescence staining using 5xFAD mice as model for AD, revealing that intracellular Aβ in these models can be diminished by TrueBlack treatment, thus confounding the interpretation of true intracellular Aβ signals. Our findings underscore the need for caution in interpreting intracellular Aβ signals in young adults and aged models of Aβ pathology inside neurons or microglia.

细胞内β淀粉样蛋白（a β）积累是阿尔茨海默病（AD）的一个有争议的特征，越来越多地在年轻成人和老年AD动物模型中报道。然而，由高度氧化的脂质、错误折叠的蛋白质和金属的混合物组成的自荧光脂褐素颗粒，随着神经元和小胶质细胞的衰老而积累，使得基于免疫荧光的研究难以解释。在这里，我们发现脂褐素在衰老野生型（WT）小鼠大脑中的积累与常用的Aβ检测抗体表现出显著的光谱重叠，导致细胞内Aβ信号的潜在误解。通过染料染色、免疫组织化学（IHC）和共聚焦显微镜的结合，我们发现类似于细胞内a β的荧光信号，通常在老年AD动物模型中报道，可能反映了脂褐素颗粒的存在。重要的是，这些信号在省略一抗Aβ抗体的对照切片中持续存在，但在TrueBlack自身荧光淬灭剂后消失。我们还使用5xFAD小鼠作为AD模型进行了Aβ免疫荧光染色，发现TrueBlack处理可以减少这些模型中的细胞内Aβ，从而混淆了对细胞内真实Aβ信号的解释。我们的研究结果强调了在解释年轻成人和老年神经元或小胶质细胞内的Aβ病理模型的细胞内Aβ信号时需要谨慎。

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引用次数: 0

Contributions of lifestyle, education, and cardiovascular risk factors to the brain age gap 生活方式、教育和心血管危险因素对大脑年龄差距的影响

IF 2.7 Q3 CLINICAL NEUROLOGY

Aging brain

Pub Date : 2025-01-01 DOI: 10.1016/j.nbas.2025.100149

Kostas Stoitsas , Pieter Bakx , Trudy Voortman , Jing Yu , Gennady Roshchupkin , Daniel Bos

The brain age gap is the difference between chronological age and the age predicted from Magnetic Resonance Imaging (MRI) brain scans. We investigated the influence of life habits and cardio-metabolic factors on this gap. A convolutional neural network (CNN) was trained on structural MRI scans from dementia-free participants in the Rotterdam Study.

Scans were collected every 3–4 years from 2005 to 2016. 10,989 images from 5,167 participants (mean age: 64 years [range: 45–98], 54 % female) were used to train and evaluate the model. We run analysis of variance and linear mixed models to assess associations between brain age gap and smoking, sleep, alcohol consumption, education, and cardio-metabolic factors.

The brain age gap in participants who developed dementia was elevated relative to cognitively healthy individuals and showed a progressive increase throughout the study period.

We found that together, the examined factors explained no more than 21% of the variance in brain age gap. Smoking, alcohol consumption, and elevated glucose levels are significantly associated with an increased brain age gap, consistent with earlier studies linking these factors to brain atrophy and cognitive decline.

脑年龄差距是指实际年龄与磁共振成像（MRI）脑部扫描预测的年龄之间的差异。我们调查了生活习惯和心脏代谢因素对这一差距的影响。在鹿特丹研究中，卷积神经网络（CNN）在无痴呆参与者的结构MRI扫描上进行了训练。从2005年到2016年，每3-4年收集一次扫描。来自5,167名参与者（平均年龄：64岁[范围：45-98岁]，54%为女性）的10,989张图像用于训练和评估模型。我们通过方差分析和线性混合模型来评估脑年龄差距与吸烟、睡眠、饮酒、教育和心脏代谢因素之间的关系。与认知健康的人相比，患有痴呆症的参与者的大脑年龄差距有所增加，并在整个研究期间逐渐增加。我们发现，这些被检查的因素加在一起，解释了不超过21%的大脑年龄差距差异。吸烟、饮酒和血糖水平升高与脑年龄差距增加显著相关，这与早期将这些因素与脑萎缩和认知能力下降联系起来的研究一致。

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引用次数: 0

Tau aggregation induces cell death in iPSC-derived neurons Tau 聚集诱导 iPSC 衍生神经元的细胞死亡

IF 1.7 Q3 CLINICAL NEUROLOGY

Aging brain

Pub Date : 2025-01-01 DOI: 10.1016/j.nbas.2025.100136

Hirokazu Tanabe , Sumihiro Maeda , Etsuko Sano , Norio Sakai , Setsu Endoh-Yamagami , Hideyuki Okano

Abnormal accumulation of tau proteins in the brain is a hallmark of neurodegenerative diseases such as Alzheimer’s disease and is closely linked with neuronal cell death. Tau accumulation is a prominent therapeutic target for Alzheimer’s disease, since tau accumulation correlates well with the disease progression, and tau-targeting drugs hold potentials to halt the disease progression. Given the differential response of human and mouse neuronal cells, there is a critical need for a human cellular platform to quickly screen for tau-related neurodegenerative disease therapeutics. However, inducing rapid, tau-dependent neuronal cell death in human models remains challenging. In this study, we established a human cellular model capable of inducing tau aggregation-dependent neuronal cell death within two weeks via tau overexpression. Additionally, we demonstrated the neuroprotective efficacy of known tau-targeting compounds within this system. These findings suggest that our cellular model recapitulates the molecular pathogenesis of tau-induced neurodegeneration and could serve as a valuable platform for drug screening in tauopathies.

大脑中 tau 蛋白的异常积累是阿尔茨海默病等神经退行性疾病的标志，与神经细胞死亡密切相关。Tau 蛋白积聚是阿尔茨海默病的一个重要治疗靶点，因为 Tau 蛋白积聚与疾病进展密切相关，而 Tau 蛋白靶向药物有可能阻止疾病进展。鉴于人类和小鼠神经细胞的反应不同，因此亟需一个人类细胞平台来快速筛选与 tau 相关的神经退行性疾病治疗药物。然而，在人类模型中诱导 tau 依赖性神经元细胞快速死亡仍具有挑战性。在这项研究中，我们建立了一种人类细胞模型，该模型能够在两周内通过tau过表达诱导tau聚集依赖性神经元细胞死亡。此外，我们还证明了已知的 tau 靶向化合物在该系统中的神经保护功效。这些研究结果表明，我们的细胞模型再现了 tau 诱导的神经退行性变的分子发病机制，可以作为筛选 tau 病药物的重要平台。

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引用次数: 0

Advanced brain aging mediates the relationship between cardiovascular health and aphasia severity in chronic stroke 脑高级老化介导慢性脑卒中患者心血管健康与失语严重程度之间的关系

IF 2.7 Q3 CLINICAL NEUROLOGY

Aging brain

Pub Date : 2025-01-01 DOI: 10.1016/j.nbas.2025.100150

Natalie Busby , Ida Rangus , Nicholas Riccardi , Roger Newman-Norlund , Chris Rorden , Julius Fridriksson , Leonardo Bonilha

Introduction

There is evidence that overall physical health in general and cardiovascular risk (CV) factors in particular are associated with structural brain changes and recovery trajectories in stroke aphasia, however the nature of these relationships is still unclear. Therefore, we investigated the mediating role of advanced brain aging on the relationship between cardiovascular health and aphasia severity in chronic stroke.

Methods

Participants (N = 95) with chronic stroke aphasia completed behavioral testing including the Western Aphasia Battery Aphasia Quotient (WAB AQ) and MRI scanning. Brain age of each participant was calculated using BrainAgeR and their proportional brain age (PBA) was calculated through the relative difference between estimated brain age and chronological age. A CV risk score was also calculated for each participant using the Framingham Heart Study General Cardiovascular Disease Risk Prediction Using BMI calculator. To determine if the relationship between vascular score and WAB AQ is related to brain age, we performed a statistical mediation analysis where the independent variable was vascular score, the dependent variable was WAB AQ and the mediating variable was PBA.

Results

Individuals with chronic stroke aphasia who had more cardiovascular risk factors (i.e., a higher vascular score), typically had worse aphasia severity (lower WAB AQ) and advanced brain aging (increased PBA). An increased PBA was also associated with worse aphasia severity. Mediation analyses revealed that individuals with a higher vascular score (i.e., worse heart health) typically had advanced brain aging and, in turn, advanced brain aging was associated with worse aphasia severity. Therefore, the total effect of cardiovascular health on aphasia severity is partially explained by the indirect effects of advanced brain aging.

Discussion

Our results corroborate the previous findings suggesting that physical health is an important factor for both brain structural integrity and recovery in stroke aphasia and extends this by demonstrating the mediating effect of advanced brain aging on the relationship between cardiovascular health and aphasia severity. These results highlight the importance of maintaining physical health alongside aphasia therapy and may be an important factor to consider in the long-term management of chronic stroke. Ensuring that individuals have access to resources needed for proper exercise and maintaining a balanced diet may help to improve overall brain structural integrity and therefore may impact aphasia severity.

有证据表明，总体身体健康，特别是心血管风险因素与脑结构变化和脑卒中失语症的恢复轨迹有关，但这些关系的本质尚不清楚。因此，我们研究脑衰老在慢性脑卒中患者心血管健康与失语严重程度之间的中介作用。方法对95例慢性脑卒中失语患者进行行为测试，包括西方失语电池失语商（WAB AQ）和MRI扫描。使用BrainAgeR计算每个参与者的脑年龄，并通过估计的脑年龄与实际年龄之间的相对差异计算他们的比例脑年龄（PBA）。还使用Framingham心脏研究一般心血管疾病风险预测使用BMI计算器计算每个参与者的CV风险评分。为了确定血管评分和WAB AQ之间的关系是否与脑年龄有关，我们进行了统计中介分析，其中自变量为血管评分，因变量为WAB AQ，中介变量为PBA。结果慢性中风失语症患者心血管危险因素较多（即血管评分较高），失语症严重程度较差（WAB AQ较低），脑老化程度较深（PBA升高）。PBA升高也与失语严重程度加重有关。中介分析显示，血管评分较高（即心脏健康状况较差）的个体通常有较严重的大脑老化，反过来，较严重的大脑老化与较严重的失语症有关。因此，心血管健康对失语严重程度的总体影响部分可以用脑衰老的间接影响来解释。我们的研究结果证实了先前的研究结果，即身体健康是脑结构完整性和脑失语症恢复的重要因素，并通过证明大脑衰老在心血管健康和失语症严重程度之间的中介作用来扩展这一点。这些结果强调了在失语治疗的同时保持身体健康的重要性，并且可能是慢性卒中长期治疗中需要考虑的一个重要因素。确保个人获得适当运动所需的资源和保持均衡的饮食可能有助于提高整体大脑结构的完整性，从而可能影响失语症的严重程度。

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引用次数: 0

Neural stem cell secretome: a secret key to unlocking the power of regeneration in the adult and aging brain 神经干细胞分泌组：解锁成人和衰老大脑再生能力的秘密钥匙

IF 1.7 Q3 CLINICAL NEUROLOGY

Aging brain

Pub Date : 2025-01-01 DOI: 10.1016/j.nbas.2025.100144

Soumia Abdellaoui , Lida Katsimpardi

Adult neurogenesis involves the activation of quiescent neural stem cells (qNSCs) to generate new neurons, which migrate and integrate into existing neural circuits. In addition to their role in neurogenesis, adult NSCs also secrete bioactive compounds collectively known as the secretome, which contribute to the regulation of this process. However, aging and neurodegenerative diseases impair neurogenesis by promoting a pro-inflammatory environment within the neurogenic niche. With age, NSCs become increasingly quiescent, leading to a decline in their secretory activity— a hallmark of aged NSCs. Enhancing the function of adult NSCs holds therapeutic potential for restoring brain function under these conditions. Specifically, reactivating quiescent NSCs and possibly eliminating senescent ones can boost neurogenesis and improve cognitive function in aging and neurodegenerative diseases. In this review, we explore the role of adult NSCs and their secretome in sustaining brain function throughout adulthood and aging. A comprehensive analysis of the literature sheds light onto how NSCs and their secretome influence neurogenesis, from activation and differentiation to integration into neural circuits. Targeting adult NSCs in aged and neurodegenerative models presents a promising strategy for brain function restoration.

成人神经发生涉及静止神经干细胞（qNSCs）的激活，以产生新的神经元，这些神经元迁移并整合到现有的神经回路中。除了在神经发生中发挥作用外，成人NSCs还分泌生物活性化合物，统称为分泌组，有助于调节这一过程。然而，衰老和神经退行性疾病通过促进神经源性生态位内的促炎环境而损害神经发生。随着年龄的增长，NSCs变得越来越安静，导致其分泌活性下降——这是衰老的NSCs的标志。增强成人NSCs的功能具有恢复这些条件下脑功能的治疗潜力。具体而言，重新激活静止的NSCs并可能消除衰老的NSCs可以促进神经发生并改善衰老和神经退行性疾病的认知功能。在这篇综述中，我们探讨了成人NSCs及其分泌组在维持成年期和衰老期脑功能中的作用。对文献的全面分析揭示了NSCs及其分泌组如何影响神经发生，从激活和分化到整合到神经回路。在老年和神经退行性模型中靶向成人NSCs是一种很有前途的脑功能恢复策略。

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引用次数: 0

Frontal theta oscillations and cognitive flexibility: Age-related modulations in EEG activity 额叶θ波振荡与认知灵活性：脑电图活动的年龄相关调节

IF 1.7 Q3 CLINICAL NEUROLOGY

Aging brain

Pub Date : 2025-01-01 DOI: 10.1016/j.nbas.2025.100142

Margarita Darna , Christopher Stolz , Hannah-Sophia Jauch , Hendrik Strumpf , Jens-Max Hopf , Constanze I. Seidenbecher , Björn H. Schott , Anni Richter

Cognitive flexibility, the ability to adapt one’s behaviour in changing environments, declines during aging. Electroencephalography (EEG) studies have implicated midfrontal theta oscillations in attentional set-shifting, a measure of cognitive flexibility. Little is known about the electrocortical underpinnings of set-shifting in aging. Here, we investigated aging effects on set-shifting performance by analysing theta power in 20 young (mean age: 22.5 ± 2.9 years) and 19 older (mean age: 69.4 ± 6.1 years) adults. Increasing shift difficulty (i.e., intra- vs. extra-dimensional shifts) elicited worse performance in both age groups, with older adults showing overall longer reaction times (RTs) and increased RT variability. Young adults exhibited amplified midfrontal theta power increases with higher shift difficulty whereas older adults showed overall lower theta power and no task-related midfrontal theta power modulation, indicating potentially distinct underlying neural mechanisms.

认知灵活性，即在不断变化的环境中适应自己行为的能力，随着年龄的增长而下降。脑电图（EEG）研究表明，中额波振荡与注意力转移有关，这是一种认知灵活性的测量方法。人们对老化过程中设置转移的电皮层基础知之甚少。在此，我们通过分析20名年轻人（平均年龄：22.5±2.9岁）和19名老年人（平均年龄：69.4±6.1岁）的theta功率来研究年龄对set-shift性能的影响。增加转换难度（即，内维度与外维度转换）在两个年龄组中都引起了更差的表现，老年人表现出更长的反应时间（RTs）和更大的RT变异性。年轻人的前额叶中波功率随着移位难度的增加而增加，而老年人的前额叶中波功率总体较低，且没有任务相关的前额叶中波功率调节，这表明潜在的不同神经机制。

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引用次数: 0

TOMM40 may mediate GFAP, neurofilament light Protein, pTau181, and brain morphometry in aging TOMM40可能在衰老过程中介导GFAP、神经丝轻蛋白、pTau181和脑形态计量学。

IF 1.7 Q3 CLINICAL NEUROLOGY

Aging brain

Pub Date : 2025-01-01 DOI: 10.1016/j.nbas.2024.100134

Robyn A. Honea , Heather Wilkins , Suzanne L. Hunt , Paul J. Kueck , Jeffrey M. Burns , Russell H. Swerdlow , Jill K. Morris

A growing amount of data has implicated the TOMM40 gene in the risk for Alzheimer’s disease (AD), neurodegeneration, and accelerated aging. No studies have investigated the relationship of TOMM40 rs2075650 (‘650) on the structural complexity of the brain or plasma markers of neurodegeneration. We used a comprehensive approach to quantify the impact of TOMM40 ‘650 on brain morphology and multiple cortical attributes in cognitively unimpaired (CU) individuals. We also tested whether the presence of the risk allele, G, of TOMM40 ‘650 was associated with plasma markers of amyloid, tau, and neurodegeneration and if there were interactions with age and sex, controlling for the effects of APOE ε4. We found that the TOMM40 ‘650 G-allele was associated with decreased sulcal depth, increased gyrification index, and decreased gray matter volume. NfL, GFAP, and pTau181 had independent and age-associated increases in individuals with a G-allele. Our data suggest that TOMM40 ‘650 is associated with aging-related plasma biomarkers and brain structure variation in temporal-limbic circuits.

越来越多的数据表明，TOMM40基因与阿尔茨海默病（AD）、神经变性和加速衰老的风险有关。尚未有研究研究TOMM40 rs2075650（'650）与脑结构复杂性或神经变性血浆标志物的关系。我们使用了一种综合的方法来量化TOMM40 '650对认知未受损（CU）个体的大脑形态和多种皮质属性的影响。我们还测试了TOMM40 '650的风险等位基因G的存在是否与淀粉样蛋白、tau蛋白和神经变性的血浆标志物相关，以及是否与年龄和性别相互作用，控制APOE ε4的影响。我们发现TOMM40 '650 g等位基因与沟深减小、旋转指数增加和灰质体积减小有关。在携带g等位基因的个体中，NfL、GFAP和pTau181具有独立的和与年龄相关的增加。我们的数据表明TOMM40 '650与衰老相关的血浆生物标志物和颞边缘回路的大脑结构变化有关。

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引用次数: 0

Testing the causal impact of plasma amyloid on total Tau using a genetically informative sample of adult male twins 使用成年男性双胞胎的遗传信息样本测试血浆淀粉样蛋白对总Tau蛋白的因果影响

IF 1.7 Q3 CLINICAL NEUROLOGY

Aging brain

Pub Date : 2025-01-01 DOI: 10.1016/j.nbas.2025.100139

Nathan A. Gillespie , Michael C. Neale , Matthew S. Panizzon , Ruth E. McKenzie , Xin M. Tu , Hong Xian , Chandra A. Reynolds , Michael J. Lyons , Robert A. Rissman , Jeremy A. Elman , Carol Franz , William S. Kremen

The amyloid cascade hypothesis predicts that amyloid-beta (Aβ) aggregation drives tau tangle accumulation. We tested competing causal and non-causal hypotheses regarding the direction of causation between Aβ40 and Aβ42 and total Tau (t-Tau) plasma biomarkers. Plasma Aβ40, Aβ42, t-Tau, and neurofilament light chain (NFL) were measured in 1,035 men (mean = 67.0 years) using Simoa immunoassays. Genetically informative twin modeling tested the direction of causation between Aβs and t-Tau. No clear evidence that Aβ40 or Aβ42 directly causes t-Tau was observed. Instead, the alternative causal hypotheses also fit the data well. In contrast, exploratory analyses suggested a causal impact of the Aβ biomarkers on NFL. Separately, reciprocal causation was observed between t-Tau and NFL. Plasma Aβ40 or Aβ42 do not appear to have a direct causal impact on t-Tau, though our use of total rather than phosphorylated tau was a limitation. In contrast, Aβ biomarkers appeared to causally impact NFL in cognitively unimpaired men in their late 60 s.

淀粉样蛋白级联假说预测淀粉样蛋白- β (Aβ)聚集驱动tau缠结积累。我们测试了关于Aβ40和Aβ42与总Tau （t-Tau）血浆生物标志物之间因果关系方向的竞争性因果和非因果假设。采用Simoa免疫测定法测定1035名男性（平均67.0岁）的血浆a - β40、a - β42、t-Tau和神经丝轻链（NFL）。遗传信息双胞胎模型测试了Aβs和t-Tau之间的因果关系方向。没有明确的证据表明Aβ40或Aβ42直接导致t-Tau。相反，其他因果假设也很符合数据。相比之下，探索性分析表明a β生物标志物对NFL有因果影响。另外，在t-Tau和NFL之间观察到反向因果关系。血浆a β40或a β42似乎对t-Tau没有直接的因果影响，尽管我们使用总tau而不是磷酸化tau是一个限制。相比之下，Aβ生物标志物似乎对60多岁的认知未受损男性的NFL有因果影响。

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引用次数: 0

Human adult hippocampal neurogenesis in health and disease 健康与疾病中的成人海马神经发生

IF 1.7 Q3 CLINICAL NEUROLOGY

Aging brain

Pub Date : 2025-01-01 DOI: 10.1016/j.nbas.2025.100145

MC. Alonso-Moreno , M. Gallardo-Caballero , AV. Prádanos-Senén , M. Llorens-Martín

The mammalian hippocampus generates new dentate granule cells (DGCs) throughout life. This process, named adult hippocampal neurogenesis (AHN), participates in hippocampal functions such as memory and mood regulation. Moreover, AHN is impaired in mouse models and patients with neurodegenerative and psychiatric disorders. Additionally, physiological aging targets AHN and the integrity of the hippocampal neurogenic niche. This perspective review aims to discuss the regulation of human AHN in patients with neurodegenerative and psychistric conditions. Moreover, we will address key adaptations of human AHN and the neurogenic niche in response to physiological aging.

哺乳动物海马在一生中产生新的齿状颗粒细胞（DGCs）。这个过程被称为成人海马神经发生（AHN），参与海马功能，如记忆和情绪调节。此外，AHN在小鼠模型和神经退行性疾病和精神疾病患者中受损。此外，生理衰老的目标是AHN和海马神经源性生态位的完整性。本综述旨在探讨人类AHN在神经退行性和精神疾病患者中的调节作用。此外，我们将讨论人类AHN和神经源性生态位对生理衰老的关键适应。

引用次数: 0

Aging brain最新文献

Introduction

Methods

Results

Discussion