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Connectomics and the neural basis of behaviour

Methods to acquire and process synaptic-resolution electron-microscopy datasets have progressed very rapidly, allowing production and annotation of larger, more complete connectomes. More accurate neuronal matching techniques are enriching cell type data with gene expression, neuron activity, behaviour and developmental information, providing ways to test hypotheses of circuit function. In a variety of behaviours such as learned and innate olfaction, navigation and sexual behaviour, connectomics has already revealed interconnected modules with a hierarchical structure, recurrence and integration of sensory streams.

Invasive neurophysiology and whole brain connectomics for neural decoding in patients with brain implants

A modularized open-source pipeline for invasive brain signal decoding bridges the gap between closed-loop neuromodulation and clinical brain–computer interface approaches in a large patient cohort.

Non-invasive brain stimulation: current and future applications in neurology

Non-invasive brain stimulation (NIBS) shows considerable promise as a therapeutic strategy for neurological and psychiatric disorders. This Review explores the role of NIBS techniques, including repetitive transcranial magnetic stimulation and transcranial electrical stimulation, for treating cognitive impairments, speech and language difficulties, and motor control deficits in people with neurodegenerative or brain lesion disorders.

Connectomics: Unraveling the Wiring of Neural Networks

Working in connectomics means creating comprehensive maps of brain and nervous system networks. Your research includes the identification and measurement of all parts of each neuron: the soma, dendrites, axonal path and branching patterns and combining that data with the synapses and gap junctions of the entire circuit.

Your microscopy challenges are extensive; submicron resolution is required over long distances inside large volumes of dense and complicated tissues.

Michael D. West

Can aging be reversed? Dr. Michael West explains telomerase, cellular immortality, stem cells, tissue regeneration, and the future of longevity.

LifeCraft Sciences:
https://lifecraftsciences.com/

In this episode, I sit down with pioneering molecular gerontologist and biotechnology entrepreneur Dr. Michael D. West to explore telomeres, telomerase, cellular senescence, stem cells, tissue regeneration, and the possibility of reversing biological aging.

One of our central topics is the groundbreaking telomerase program West founded and led at Geron. That research helped establish how restoring telomerase activity can protect the ends of chromosomes and allow normal human cells to move beyond their usual replicative limit while retaining youthful characteristics in laboratory culture. We unpack what scientists mean when they say a cell has been “immortalized,” why cellular immortality is very different from making a person immortal, and how telomerase connects the biology of aging with the biology of cancer.

We also explore West’s work in regenerative medicine and his early vision of pluripotent stem cells as a “parts supply store” for the human body. Could youthful cells eventually be used to repair damaged tissues, replace worn-out biological components, and restore regenerative capabilities lost with age? West discusses the early isolation of human embryonic stem cells, therapeutic cloning, developmental reprogramming, and what cloned animals taught researchers about resetting cellular age.

Finally, we discuss LifeCraft Sciences and RESTORE, the company’s experimental approach combining telomerase with developmental regulators to return aged cells to a more youthful, regenerative state. It is a fascinating conversation about the history of longevity science, the future of tissue repair, and one of biology’s biggest questions: can aging eventually be reversed rather than merely slowed?

Hope for spinal injuries as pigs walk again after experimental gel treatment for severed spinal cords

In humans and other mammals, spinal cord injuries can be devastating, leading to permanent loss of movement, sensation and bladder control. When severed axons (the long fibers that carry messages between nerve cells) cannot regrow, a dense scar forms, preventing nerve signals from passing the injury site.

But the situation is different for some primitive invertebrates, which can rapidly reconnect severed nerves by fusing them. Inspired by this natural phenomenon, scientists led by Michael Lebenstein-Gumovski at the Sklifosovsky Institute for Emergency Medicine in Russia report that they have successfully reconnected severed spinal cords in pigs, enabling them to walk again.

When a spinal cord is completely cut, the two severed ends naturally pull away from each other. In microscopic roundworms, for example, the nerve ends automatically find each other and fuse together. The researchers realized that to recreate a natural fusion process like this, they needed a material to fill the empty space and hold the two ends together.

Bridging ADHD and Metabolic Disorders: Insights into Shared Mechanisms and Clinical Implications

Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by inattention, impulsivity and/or hyperactivity. In recent years, metabolic alterations, primarily obesity, insulin resistance, and diabetes, have emerged as frequent comorbidities in individuals with ADHD, suggesting a bidirectional relationship between neurodevelopmental and metabolic dysfunctions. Emerging evidence indicates that dysregulation of dopaminergic signaling, disturbances in the hypothalamic-pituitary-adrenal (HPA) axis, and chronic low-grade inflammation are central to both ADHD symptomatology and metabolic impairments. For instance, alterations in dopamine-related genes (e.g., DRD4, DAT1) not only affect cognitive and behavioral functions but also play a role in appetite regulation and glucose homeostasis. Epidemiological studies further demonstrate that individuals with ADHD exhibit poorer glycemic control and a higher prevalence of both type 1 and type 2 diabetes, while early-life metabolic challenges such as maternal diabetes may predispose offspring to ADHD. This review aims to comprehensively synthesize the epidemiological, genetic, and pathogenetic evidence linking ADHD to metabolic alterations. We discuss key pathophysiological pathways—including dopaminergic dysregulation, HPA axis disturbances, inflammation, and oxidative stress—and evaluate their contributions to the co-occurrence of ADHD and metabolic disorders. In addition, we explore the clinical implications and integrated treatment approaches that encompass lifestyle modifications, pharmacological therapies, and multidisciplinary care. Finally, we outline future research directions to develop personalized and holistic interventions.

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