Axon regeneration can be induced across anatomically complete spinal cord injury (SCI), but robust functional restoration has been elusive. Whether restoring neurological functions requires directed regeneration of axons from specific neuronal subpopulations to their natural target regions remains unclear. To address this question, we applied projection-specific and comparative single-nucleus RNA sequencing to identify neuronal subpopulations that restore walking after incomplete SCI. We show that chemoattracting and guiding the transected axons of these neurons to their natural target region led to substantial recovery of walking after complete SCI in mice, whereas regeneration of axons simply across the lesion had no effect. Thus, reestablishing the natural projections of characterized neurons forms an essential part of axon regeneration strategies aimed at restoring lost neurological functions.
Category: neuroscience – Page 4
Wenzhou Medical University and collaborating institutions have identified a population of human neural retinal stem-like cells able to regenerate retinal tissue and support visual recovery.
Vision loss caused by retinal degeneration affects millions worldwide. Conditions such as retinitis pigmentosa and age-related macular degeneration involve the irreversible loss of light-sensitive neural cells in the retina. While current treatments may slow progression, they do not replace damaged tissue.
For decades, scientists have explored whether stem cells could be used to regenerate the retina, but the existence of true retinal stem cells in humans has remained uncertain. In fish and amphibians, the outer edge of the retina houses stem cells that regenerate tissue continuously. Whether a comparable system exists in the human eye has been debated for more than two decades.
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Mitochondria play a crucial role in maintaining energy balance and cellular health. Recent studies have shown that chronic stress in neuronal mitochondria can have far-reaching effects, not only damaging the neurons themselves but also influencing other tissues and systemic metabolic functions.
A new study led by Dr. Tian Ye’s research team at the Institute of Genetics and Developmental Biology of the Chinese Academy of Sciences (CAS) reveals that chronic mitochondrial stress in neurons promotes serotonin release via TMBIM-2-dependent calcium (Ca²⁺) oscillations, which in turn activates the mitochondrial unfolded protein response (UPRmt) in the intestine. The findings are published in the Journal of Cell Biology.
The researchers found that TMBIM-2 works in coordination with the plasma membrane calcium pump MCA-3 (a PMCA homolog) to regulate synaptic Ca²⁺ balance, sustaining persistent calcium signaling oscillations at neuronal synaptic sites.
Your brain burns 20 percent of your body’s energy and now we know exactly where it goes.
Research findings focus on people with a sleep disorder, but could have broader implications. For people with a certain sleep disorder, a simple blood test could help predict the development of dementia years before symptoms appear, a new study indicates.
Idiopathic REM sleep behaviour disorder (iRBD) causes people to physically act out their dreams while sleeping.
The disorder is also associated with a very high risk of Parkinson’s disease and a related condition called Dementia with Lewy Bodies.
A standard commercial CMOS FET can exhibit synaptic-like long-term potentiation and depression or neuron-like leaky-integrate-and-fire and adaptive frequency-bursting behaviour when biased in a specific but unconventional way.
New in JNeurosci: In a study comparing human brains to macaque and chimpanzee brains, Bryant et al. discovered neuroanatomical features that are unique to humans.
Learn more. ▶️
Determining the brain specializations unique to humans requires directly comparative anatomical information from other primates, especially our closest relatives. Human (Homo sapiens) (m/f), chimpanzee (Pan troglodytes) (f), and rhesus macaque (Macaca mulatta) (m/f) white matter atlases were used to create connectivity blueprints, i.e., descriptions of the cortical grey matter in terms of the connectivity with homologous white matter tracts. This allowed a quantitative comparative of cortical organization across the species. We identified human-unique connectivity profiles concentrated in temporal and parietal cortices, and hominid-unique organization in prefrontal cortex. Functional decoding revealed human-unique hotspots correlated with language processing and social cognition. Overall, our results counter models that assign primacy to prefrontal cortex for human uniqueness.
Significance statement Understanding what makes the human brain unique requires direct comparisons with other primates, particularly our closest relatives. Using connectivity blueprints, we compared to cortical organization of the human to that of the macaque and, for the first time, the chimpanzee. This approach revealed human-specific connectivity patterns in the temporal and parietal lobes, regions linked to language and social cognition. These findings challenge traditional views that prioritize the prefrontal cortex in defining human cognitive uniqueness, emphasizing instead the importance of temporal and parietal cortical evolution in shaping our species’ abilities.
The authors show that neuroprotective and neurotoxic astrocytes representional cellular substates present during neuroinflammation and that targeting mTOR in astrocytes reduces neurotoxicity, suggesting a potential therapeutic strategy for neurodegenerative diseases.
Reelin is a critical mechanistic link between neuronal activation and cocaine-induced behavioral adaptations.