Diffusion tensor imaging of white matter tract evolution over the lifespan

Lebel, Catherine; Gee, Myrlene; Camicioli, Richard; Wieler, Marguerite; Martin, W. R. Wayne; Beaulieu, Christian

doi:10.1016/j.neuroimage.2011.11.094

Cited by 982 publications

(1,130 citation statements)

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“…This study also comes with the limitations inherent to large crosssectional datasets across the lifespan, such as possible cohort effects and selection bias, which might influence the age peak to some degree (31). Various imaging studies support a similar timeline for late development (32)(33)(34)(35), however, while recent cellular findings show, for instance, that myelination and remodeling of synaptic spines extend later than previously thought, beyond adolescence and young adulthood (36,37).…”

Section: Discussionmentioning

confidence: 82%

A common brain network links development, aging, and vulnerability to disease

Douaud

Groves

Tamnes³

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

300

263

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Several theories link processes of development and aging in humans. In neuroscience, one model posits for instance that healthy agerelated brain degeneration mirrors development, with the areas of the brain thought to develop later also degenerating earlier. However, intrinsic evidence for such a link between healthy aging and development in brain structure remains elusive. Here, we show that a data-driven analysis of brain structural variation across 484 healthy participants (8-85 y) reveals a largely-but not only-transmodal network whose lifespan pattern of age-related change intrinsically supports this model of mirroring development and aging. We further demonstrate that this network of brain regions, which develops relatively late during adolescence and shows accelerated degeneration in old age compared with the rest of the brain, characterizes areas of heightened vulnerability to unhealthy developmental and aging processes, as exemplified by schizophrenia and Alzheimer's disease, respectively. Specifically, this network, while derived solely from healthy subjects, spatially recapitulates the pattern of brain abnormalities observed in both schizophrenia and Alzheimer's disease. This network is further associated in our large-scale healthy population with intellectual ability and episodic memory, whose impairment contributes to key symptoms of schizophrenia and Alzheimer's disease. Taken together, our results suggest that the common spatial pattern of abnormalities observed in these two disorders, which emerge at opposite ends of the life spectrum, might be influenced by the timing of their separate and distinct pathological processes in disrupting healthy cerebral development and aging, respectively.M any phylogenetic or ontogenetic models attempt to relate development and aging at genetic, molecular, or cognitive systems levels (1-4). In neuroscience, one of the most popular hypotheses in this respect postulates that the process of healthy age-related brain decline mirrors developmental maturation. This concept was first introduced in 1881 as a "loi de régression" (Ribot's law) when Théodule Ribot, a French philosopher, observed that the destruction of memories progresses in reverse order to that of their formation: from the unstable to the stable, from the newly formed memories to older "sensory, instinctive" memories (5). More generally, this hypothesis postulates that the sequence of events associated with brain decline should present itself in reverse order to the series of events related to brain development, with brain regions thought to develop relatively late-at both ontogenetic and phylogenetic levels-also degenerating relatively early (2, 6, 7).One way of tracking this hypothesized mirroring pattern of development and aging in the human brain is to use the information provided at a macroscopic level by structural MRI in large-scale, lifespan human populations. Although structural MRI does not distinguish between the various cellular mechanisms underpinning development and aging processes [e.g., de...

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Section: Discussionmentioning

confidence: 82%

A common brain network links development, aging, and vulnerability to disease

Douaud

Groves

Tamnes³

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

300

263

View full text Add to dashboard Cite

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“…In humans, we examined connectivity within the uncinate fasciculus (UF), a white matter tract in the human brain that connects limbic structures in the anterior temporal lobe with ventral and medial prefrontal cortices (21)(22)(23)(24) implicated in anxiety (15). This fiber bundle shows a protracted developmental trajectory, with continuing development well into young adulthood (25,26). We measured fractional anisotropy (FA), an index of connectivity derived from diffusion tensor imaging, and controlled for sex, ancestry, and site (i.e., imaging facility at which the scan occurred).…”

Section: Faah C385a-associated (Phenotypic) Differences In Frontolimbmentioning

confidence: 99%

Individual differences in frontolimbic circuitry and anxiety emerge with adolescent changes in endocannabinoid signaling across species

Gee

Fetcho

Jing

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Anxiety disorders peak in incidence during adolescence, a developmental window that is marked by dynamic changes in gene expression, endocannabinoid signaling, and frontolimbic circuitry. We tested whether genetic alterations in endocannabinoid signaling related to a common polymorphism in fatty acid amide hydrolase (FAAH), which alters endocannabinoid anandamide (AEA) levels, would impact the development of frontolimbic circuitry implicated in anxiety disorders. In a pediatric imaging sample of over 1,000 3-to 21-y-olds, we show effects of the FAAH genotype specific to frontolimbic connectivity that emerge by ∼12 y of age and are paralleled by changes in anxietyrelated behavior. Using a knock-in mouse model of the FAAH polymorphism that controls for genetic and environmental backgrounds, we confirm phenotypic differences in frontoamygdala circuitry and anxiety-related behavior by postnatal day 45 (P45), when AEA levels begin to decrease, and also, at P75 but not before. These results, which converge across species and level of analysis, highlight the importance of underlying developmental neurobiology in the emergence of genetic effects on brain circuitry and function. Moreover, the results have important implications for the identification of risk for disease and precise targeting of treatments to the biological state of the developing brain as a function of developmental changes in gene expression and neural circuit maturation.A nxiety disorders typically emerge during adolescence, when the incidence of mental illness peaks (1, 2). The developmental phase of adolescence is characterized by dynamic changes in gene expression, frontolimbic circuitry (3, 4), and overall tone of the endocannabinoid system, which are implicated in anxiety (5-7).The corticolimbic endocannabinoid system undergoes dynamic changes across development. The onset of adolescence is marked by the highest expression of type 1 cannabinoid receptor (CB1) in both cortical and subcortical brain regions, with CB1 expression declining to adult levels throughout adolescence (8, 9). Across the amygdala and prefrontal cortex, fatty acid amide hydrolase (FAAH) expression shows a transient increase from postnatal day 35 (P35) to P45 during adolescence in mice (10). Consistent with the regulatory role of FAAH, anandamide (AEA) levels show an inverse pattern of a peak at P35 and subsequent decrease during adolescence (10, 11). AEA is an endogenous ligand for the CB1 receptor, suggesting that the concurrent changes in AEA and CB1 expression reflect decreasing endocannabinoid signaling during adolescence (12), which may be associated with increasing risk for anxiety (Fig. 1).A common human polymorphism in the gene encoding FAAH (C385A; rs324420), the primary catabolic enzyme of the prototypical endocannabinoid AEA, regulates FAAH activity. The variant FAAH A385 allele destabilizes the FAAH protein, causing lower levels of FAAH enzymatic activity and/or increased levels of AEA in T lymphocytes and brain (13,14). Phenotypic expression of common polymorphism...

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“…17 Axonal myelination continues through adolescence into the early 20s, and is susceptible to disruption by injury. 10,[18][19][20][21][22] Early results from the Professional Fighters Brain Health Study, a 5-year longitudinal study of boxers and mixed martial arts fighters, who experienced repetitive subconcussive injuries as well as concussions, indicate that earlier age of first exposure to competitive boxing correlates with greater loss of caudate volume and greater axonal damage in the frontal lobe. 23,24 The young brain also has features that contribute to its resilience.…”

Section: Susceptibility and Resilience Of Young Brainsmentioning

confidence: 99%