Neuroscience

Stroke, TBI, and Alzheimer's/Parkinson's differ in cause but converge on the same breakdown pathways. Why don't NGF and BDNF work in humans? A Russian team reads the delivery barrier from six trials.

A tadpole whose spinal cord is severed will regenerate; after metamorphosis, the same frog cannot, and its response closely resembles that of humans. In Chile, Dr. Slater and colleagues showed that on the non-regenerating side, mitochondria swell by day 6 after injury, cristae turn into vesicles, and the respiratory enzyme COX shuts down. Yet ATP did not fall — it rose. Genes for glycolysis and genes that mobilize fat were both switched on. That said, the extra ATP may simply have leaked out of damaged tissue. Dr. Exotaro reads this preclinical frog study.

A man paralyzed from the neck down can now move his own hand by thought alone and even feel the texture of what he grips. A team at the Feinstein Institutes for Medical Research has developed a 'double neural bypass (DNB)' that bridges the brain to the spinal cord and cortex at the same time. While the device is on, it takes over hand movement and touch (assist); through electrical-stimulation training it also drew out recovery that persists even after the device is switched off (therapy). Cracking an egg without breaking it, feeding himself, feeling a dog's fur again through a once-paralyzed wrist—Dr. Exotaro unpacks this landmark first-in-human study.

Exercise reaches the brain through peripheral signals—BDNF, lactate, immune and vascular messengers. But a biomarker "moving" is not the same as cognition returning. An Italian neurorehabilitation team offers an integrative model: the biological effects of exercise become clinically meaningful only when they couple to attention-demanding movement and surface as a behavior called cognitive-motor integration (CMI). Exotaro unpacks a review that surveys the differences across stroke, Parkinson's, MS, and TBI, and how to deploy VR, robots, and wearables.

Using the zebrafish brain, this study reveals the crucial role that degradation of the extracellular matrix (ECM) plays in synaptic plasticity during brain development.

GLP-1 receptor agonists (GLP-1RA), approved for type 2 diabetes (T2D), obesity, and cardiovascular disease, are now drawing attention as potential therapies for Alzheimer's disease (AD).