Dataset Information

Functional connectome through the human life span.

ABSTRACT: The functional connectome of the human brain represents the fundamental network architecture of functional interdependence in brain activity, but its normative growth trajectory across the life course remains unknown. Here, we aggregate the largest, quality-controlled multimodal neuroimaging dataset from 119 global sites, including 33,809 task-free fMRI and structural MRI scans from 32,328 individuals ranging in age from 32 postmenstrual weeks to 80 years. Lifespan growth charts of the connectome are quantified at the whole cortex, system, and regional levels using generalized additive models for location, scale, and shape. We report critical inflection points in the non-linear growth trajectories of the whole-brain functional connectome, particularly peaking in the fourth decade of life. Having established the first fine-grained, lifespan-spanning suite of system-level brain atlases, we generate person-specific parcellation maps and further show distinct maturation timelines for functional segregation within different subsystems. We identify a spatiotemporal gradient axis that governs the life-course growth of regional connectivity, transitioning from primary sensory cortices to higher-order association regions. Using the connectome-based normative model, we demonstrate substantial individual heterogeneities at the network level in patients with autism spectrum disorder and patients with major depressive disorder. Our findings shed light on the life-course evolution of the functional connectome and serve as a normative reference for quantifying individual variation in patients with neurological and psychiatric disorders.

SUBMITTER: Sun L

PROVIDER: S-EPMC10515818 | biostudies-literature | 2023 Sep

REPOSITORIES: biostudies-literature

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Functional connectome through the human life span.

Sun Lianglong L Zhao Tengda T Liang Xinyuan X Xia Mingrui M Li Qiongling Q Liao Xuhong X Gong Gaolang G Wang Qian Q Pang Chenxuan C Yu Qian Q Bi Yanchao Y Chen Pindong P Chen Rui R Chen Yuan Y Chen Taolin T Cheng Jingliang J Cheng Yuqi Y Cui Zaixu Z Dai Zhengjia Z Deng Yao Y Ding Yuyin Y Dong Qi Q Duan Dingna D Gao Jia-Hong JH Gong Qiyong Q Han Ying Y Han Zaizhu Z Huang Chu-Chung CC Huang Ruiwang R Huo Ran R Li Lingjiang L Lin Ching-Po CP Lin Qixiang Q Liu Bangshan B Liu Chao C Liu Ningyu N Liu Ying Y Liu Yong Y Lu Jing J Ma Leilei L Men Weiwei W Qin Shaozheng S Qiu Jiang J Qiu Shijun S Si Tianmei T Tan Shuping S Tang Yanqing Y Tao Sha S Wang Dawei D Wang Fei F Wang Jiali J Wang Pan P Wang Xiaoqin X Wang Yanpei Y Wei Dongtao D Wu Yankun Y Xie Peng P Xu Xiufeng X Xu Yuehua Y Xu Zhilei Z Yang Liyuan L Yuan Huishu H Zeng Zilong Z Zhang Haibo H Zhang Xi X Zhao Gai G Zheng Yanting Y Zhong Suyu S He Yong Y

bioRxiv : the preprint server for biology 20240610

The lifespan growth of the functional connectome remains unknown. Here, we assemble task-free functional and structural magnetic resonance imaging data from 33,250 individuals aged 32 postmenstrual weeks to 80 years from 132 global sites. We report critical inflection points in the nonlinear growth curves of the global mean and variance of the connectome, peaking in the late fourth and late third decades of life, respectively. After constructing a fine-grained, lifespan-wide suite of system-leve ...[more]

PMID: 37745373

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Project description:ABSTRACT MAGWIRE, MICHAEL MAHLON. Mutations Increasing Drosophila melanogaster Life Span. (Under the direction of Trudy F. C. Mackay.) Better living conditions and advances in medicine have made it possible for humans to live considerably longer than before. This has uncovered many health problems associated with age. By identifying genes involved in the limitation of life span, we may better understand the processes that lead to aging. In model organisms, we can use mutagenesis to discover mutations that increase life span, and hence infer that the wild-type allele limits life span by some means. We have assessed longevity in a collection of 1332 co-isogenic gene-trap P-element insertion lines and determined changes in life span of each insert line relative to the corresponding control line. Significant lines were determined via two different methods of analysis: A 95% confidence interval was established based on deviations of the mutant life spans from the controls and Dunnett’s two tailed t-tests were used to examine differences between mutant and control in each individual block. Based on the 95% confidence interval, 139 inserts displayed an increase in life span and 194 inserts a decrease. Using Dunnett’s, 70 lines increased in life span, while 270 decreased in life span. An additional 48 increased longevity lines were close enough to meeting Dunnett’s criteria to be considered for additional investigation. Combining these two analyses, we chose 83 inserts associated with increased life span for a secondary screen using an additional twelve replicates. 58 of these lines remained significant. We have determined the P-element insertion site for 50 of these lines. Starvation resistance, chill coma recovery time and climbing activity were measured on the lines remaining significant after the the secondary screen to identify pleiotropic effects. A positive correlation was found for males between life span and starvation resistance as well as between life span and chill coma recovery. Females only displayed a correlation between life span and chill coma recovery, which was negative. None of the lines indicated increased fitness for all phenotypes, indicating there may be some type of trade-off. There also appears to be a lot of pleiotropic variation depending on background and sex. Ten of the lines, all with the same parental background, were chosen for a half-diallel cross to identify epistasis between the mutants. There were substantial epistatic interactions between all ten lines. Furthermore, males and females displayed vastly different patterns of epistasis, again indicating major differences in life span regulation between the sexes. Finally, a subset of seven of the lines used in the epistatic study, in addition to the corresponding parental control, were chosen for microarray analysis to look for possible pathways and novel genes involved in increasing life span. 1,996 probe sets were significant at a false discovery rate q-value threshold of q < 0.0001. Tukeys tests were carried out for these probe sets to determine how each of the seven mutant backgrounds differed compared to the control and each other. In addition, each mutant background was compared individually with the control to identify any changes in expression. Gene ontologies were determined for each of the lines to identify over-represented biological functions which would indicate possible longevity pathways. Dozens of pathways were suggested, including several novel pathways. Keywords: Genetic (P-element insertion) modification and comparison to control line

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Functional connectome through the human life span.

Publications

Functional connectome through the human life span.

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