Your brain’s “stop eating” signal may come from an unexpected source. Researchers found that astrocytes—once thought to just support neurons—actually play a key role in controlling appetite. After a meal, glucose triggers tanycytes, which send signals to astrocytes that then activate fullness neurons. This newly discovered pathway could lead to innovative treatments for obesity and eating disorders.
Debates over how geometry is understood and learned date back at least to the days of Plato, with more recent scholars concluding that only humans possess the foundations of this understanding. However, a new analysis by New York University psychology professor Moira Dillon concludes that geometry’s foundations are shared by humans and a variety of other animals—from rats to chickens to fish.
“Our ability to think geometrically may not come from a built-in, uniquely human ‘math module’ in the brain, but rather from the same cognitive systems that help humans, as well as animals, find their way home,” explains Dillon, whose work appears in the journal Trends in Cognitive Sciences. “Put another way, our understanding of geometry may very well come from wandering rather than from worksheets.”
While Plato and, later, Descartes and Kant all debated the origins of geometry and the role of cognition in its beginnings, only in the latter half of the 20th century did scientists start testing how it is learned.
Astrocyte plasticity in learning and memory.
Neuronal hallmark features of learning and memory, such as activity dependent plasticity, circuit-level modulation, and gene regulatory mechanisms, are also observed in astrocytes.
Astrocytic calcium displays plastic, activity-dependent recruitment and refinement (akin to neuronal activity) across neuronal subtypes, brain regions, and behavioral paradigms, and Designer Receptors Exclusively Activated by Designer Drugs (DREADDs)-mediated manipulations highlight astrocytic recruitment of circuit-specific neurons.
Astrocyte peripheral processes display activity-dependent plasticity and are able to discriminate between neuronal subtypes, circuits, and even individual synapses.
Single-cell RNA sequencing reveals molecularly defined subtypes of astrocytes that display unique transcriptional responses to learning and memory and implicates potential ‘ensemble’-like networks of astrocytes. sciencenewshighlights ScienceMission https://sciencemission.com/astrocyte-plasticity
Learning and memory arise from coordinated activity-dependent plasticity across neural circuits and brain regions. Astrocytes are increasingly recognized as active contributors to learning and memory via their roles in sensing, integrating, and responding to contextual information. Astrocytes modulate synaptic transmission, engage in circuit-specific signaling, and display context-dependent calcium dynamics that influence behavior. In this review, we focus on astrocyte functions across rodent models that display plasticity traditionally ascribed to neurons, including activity-dependent molecular and structural plasticity, circuit-level modulation, ensemble-like networks, and transcriptional, translational, proteomic, and epigenetic plasticity.
Researchers have developed a novel compound that could transform the way we treat Alzheimer’s disease, offering not just a new weapon but potentially a new strategy for battling the most common form of dementia worldwide.
While current drugs for Alzheimer’s mostly focus on removing amyloid-beta plaques associated with the disease, the new compound takes a fundamentally different approach, instead targeting a specific enzyme to therapeutically reprogram the epigenome of neurons – a series of molecular marks that can be added to or removed from DNA, to change the way genes work.
Monoclonal antibody drugs such as lecanemab and donanemab, which target amyloid-beta proteins, help somewhat to slow the progression of the disease when treatment is started early, but there is still no proven way to reverse cognitive decline from Alzheimer’s in humans.
In a phase 3 randomized clinical trial of adults with ParkinsonDisease experiencing motor fluctuations despite stable levodopa therapy, adjunctive tavapadon—a once-daily, selective D1/D5 dopamine agonist—significantly increased daily on-time without troublesome dyskinesia and reduced off-time compared with placebo over 27 weeks.
Most adverse events, including nausea, dyskinesia, and dizziness, were mild to moderate. Tavapadon showed a favorable safety profile and provided clinically meaningful motor improvements as adjunctive therapy.
Question Can adjunctive tavapadon—an oral, once-daily, selective dopamine (D) D1/D5 agonist—improve motor control for people with Parkinson disease (PD) experiencing motor fluctuations while minimizing risk of adverse events?
Findings In this phase 3, double-blind, placebo-controlled, 27-week randomized clinical trial of 507 participants with PD, tavapadon significantly increased daily on-time without troublesome dyskinesia (good-on-time) vs placebo. Most adverse events were mild to moderate in severity with nausea, dyskinesia, and dizziness most common with tavapadon.
Meaning Results show that tavapadon adjunctive to levodopa provided clinically meaningful motor improvements and an acceptable safety profile in adults with PD experiencing motor fluctuations while receiving oral levodopa.
Developing tau tangles doesn’t mean a person has Alzheimer’s disease – in fact, it happens to nearly everyone to varying degrees. But because these changes start in the locus coeruleus, some brain researchers – myself included – see this area as a canary in the coal mine for developing Alzheimer’s disease.
We are exploring whether stopping or slowing down tau tangles in this brain region, or otherwise maintaining its health, may be a way to interrupt how the disease ultimately unfolds and to prevent other aspects of cognitive aging.
Emerging research from my lab and others is investigating the idea that a therapy called vagus nerve stimulation, which is already widely used for other health conditions, could be one way of keeping the locus coeruleus functioning properly.
In this multicenter randomized clinical trial, 24 months of moderate to vigorous aerobic exercise, intensive pharmacological reduction of blood pressure and serum LDL cholesterol, or the combination of these interventions did not significantly improve global cognitive function compared to usual care in older adults with hypertension and either family history of dementia or subjective cognitive decline.
Exercise and intensive vascular risk reduction each improved cardiovascular parameters, but no group differences were observed for changes in the Preclinical Alzheimer Cognitive Composite or NIH Toolbox Cognition Battery scores.
Question Can exercise, intensive pharmacological reduction of blood pressure (BP) and serum low-density lipoprotein cholesterol (LDL-C), or the combination of these interventions improve cognitive function in older adults with family history of dementia and/or self-reported subjective cognitive decline?
Findings In this randomized clinical trial of 513 participants, moderate to vigorous aerobic exercise training, intensive pharmacological lowering of BP and serum LDL-C, or both did not result in statistically significant differences in improvements in global cognitive function over 24 months.
Meaning The findings do not provide evidence in support of exercise, intensive reduction of BP and serum LDL-C, or both for improving cognitive function in older adults with family history of dementia and/or self-reported subjective cognitive decline.