All articles tagged with #brain development
New research indicates laughter strengthens children's developing brains, boosts emotional bonds with caregivers, lowers stress hormones, and enhances learning by engaging memory and executive functions, with playful, shared humor in home and classroom settings helping kids navigate stress and improve resilience.
New research argues laughter is a complex brain mechanism that precedes speech, lowers stress hormones, increases happiness chemicals, and drives neuroplastic changes across a distributed brain network. When shared between parent and child, it boosts oxytocin and neural synchrony, strengthening emotional bonds and reducing burnout, while also making learning easier by lowering cognitive load. The findings suggest humor should be a central tool in early education and parenting to support resilience and lasting memory.
A large longitudinal study using ABCD data shows ADHD symptom paths in adolescence—persistent, remitting, emergent, and control—map to distinct brain development signs. Persistent symptoms link to faster cortical thinning in frontal areas; emergent symptoms to slower thinning in the right posterior cingulate; remitting symptoms to faster left hippocampal growth. A machine-learning model with baseline brain data predicted symptom severity three years later and was replicated in European adult samples. Medication did not reliably predict remission; findings point to brain-based biomarkers and non-pharmacological interventions like aerobic exercise, while acknowledging observational limitations.
A new analysis of the ABCD longitudinal dataset (11,000+ youths) shows that the long-standing claim that brains of kids with ADHD mature more slowly is likely a mirage. When researchers accounted for sex differences in how boys’ and girls’ brains develop over time, the previously observed link between ADHD and delayed cortical thinning disappeared. The finding suggests ADHD remains a biological condition with genetic components, but that early brain-imaging signals lacked reliable diagnostic biomarkers and highlighted replication challenges in neuroscience.
A new analysis challenges the long-standing claim that brains of children with ADHD mature more slowly than those of their peers. By reexamining the data with more robust methods, researchers conclude that the landmark finding was likely a mirage caused by artifacts or biases in the data, suggesting ADHD brain maturation may proceed on a timeline similar to neurotypical development.
A Nature Communications study in mice shows the hippocampus is densely wired at birth and progressively prunes connections to form mature networks, supporting a tabula plena (not a blank slate) model of brain development; the research also notes human applicability remains to be tested.
A mouse study from ISTA shows the hippocampal CA3 network is densely connected and seemingly random at birth, then prunes into a more structured circuit as the animal matures. This supports a pruning model where the brain is born “full” and optimized over time, potentially enabling faster integration of sensory information, though it’s not yet clear if humans follow the same pattern. The findings come from developmental stages spanning birth to adulthood and were published in Nature Communications.
A Nature Communications study in mice shows the hippocampal CA3 region is densely wired shortly after birth and undergoes rapid pruning into sparser, more structured networks by adolescence, suggesting early memories may be vague or prenatal wiring—not a blank slate—and that infancy benefits from preexisting, cross-modal wiring that becomes more selective with age.
Across seven decades of observations and a major 2018 study, scientists have repeatedly found that people born blind due to cortical (brain) damage do not develop schizophrenia, unlike those who become blind later or whose blindness comes from eye disease. The protection seems tied to how the visual cortex is repurposed early in life, potentially stabilizing the brain’s predictive processing and reducing misfired predictions that underlie psychosis. Timing matters: loss of vision later in life doesn’t confer the same protection. These findings point to new directions for treatment that could target perception, learning, and brain circuits (including glutamate systems in the visual cortex) alongside traditional dopamine-focused approaches, though blindness is not a practical safeguard. This line of research deepens our understanding of brain development and the origins of schizophrenia.”
Scientists mapped glucose in the developing brain and found that high local glucose drives oligodendrocyte progenitor cell (OPC) proliferation via nuclear acetyl-CoA produced by the enzyme ACLY, while lower glucose cues these cells to mature into myelin-forming oligodendrocytes. In ACLY-deficient mice, ketogenic diets can partially rescue myelin deficits by providing an alternative fuel source. This reveals a metabolic switch that times and regionalizes myelin formation during a critical late-gestation window (roughly 32–40 weeks in humans), with implications for premature white-matter injury and potential myelin-repair strategies in diseases like multiple sclerosis.
A large, longitudinal study of 11,036 U.S. youths aged about 9–10 to 16–17 found that cannabis use during adolescence is linked to slower development across memory, attention, and processing speed, with THC exposure driving most of the effects and CBD exposure showing relatively normal scores. While causality can’t be proven, researchers controlled for family background, mental health, and other substances, suggesting that delaying cannabis use may help protect the developing brain. The findings come from the ABCD study and were published in Neuropsychopharmacology, with even small cognitive differences potentially affecting learning, standardized testing, and daily functioning.
A UC San Diego-led analysis of more than 11,000 youths finds that teens who begin using cannabis show slower gains in memory, attention and processing speed over time, with THC exposure associated with worse memory; CBD exposure showed no clear pattern. The researchers caution that causality isn’t proven and will continue tracking participants into young adulthood to understand long-term effects.
Researchers tracking 85 people with 22q11.2 deletion syndrome over 25 years found that impaired brain waste clearance (glymphatic function) in childhood is linked to later psychosis. Those who developed psychotic symptoms showed weaker glymphatic development (lower ALPS index) and an excitatory/inhibitory imbalance, suggesting brain-cleaning failures early in life may contribute to psychosis and could offer avenues for preventive interventions.
A large-scale lifespan study maps three core functional gradients—sensory–association (SA), visual–somatosensory (VS), and modulation–representation (MR)—across birth to 100 years, showing early anchoring to primary sensory systems, differentiation along association and control axes through development, and later dedifferentiation with aging; these gradients relate to cognitive performance, structure–function coupling, and transcriptomic patterns, providing a normative lifespan atlas for brain organization.
A Cambridge-led study analyzed MRI diffusion scans from 3,802 people—from newborns to age 90—identifying four major turning points that divide life into five brain-wiring eras: birth to about age 9, adolescence to about 32, adulthood, early aging around 66, and late aging around 83. The evolving neural wiring correlates with changes in learning, memory, and intelligence, suggesting the brain’s development and aging follow a staged timeline that could inform education and elder care.