Mitochondrial dynamics are mainly regulated by dynamin-related protein 1 (Drp1). The molecular mechanisms that affect the functioning of Drp1 influence brain development. But little has been known on how exactly this happens. A recent study1 describes a newly discovered protein in the brain that helps regulate Drp1 and thus, brain function. The finding offers new perspective on the pathology of many developmental and neurological disorders, which could help design effective treatments and therapies for diseases like Alzheimer’s and Parkinson’s in the future.
Evie Walker sits on Alison’s lap, playing a game she never grows tired of: turning her mum’s hand over and over, stroking and examining it. When she takes a break and looks around, it is with the open-mouthed look of curiosity and awe that you see in many infants. Evie’s vocabulary currently consists of a repertoire of squawks and “mmm” sounds. In the past few months, she has begun to stand unaided for short periods – even taking a few steps in her walking frame – progress that fills her parents with immeasurable pride, not to mention hope for the future.
Microglia play a protective role in a mouse model of amyotrophic lateral sclerosis (ALS), according to new preclinical studies from Mayo Clinic scientists and collaborators1. The finding could provide a potential therapeutic target for the disease. The loss of neurons characterizes the neurodegenerative diseases of Alzheimer’s and ALS. In Alzheimer’s, the lost neurons handle memory retrieval, and in ALS, it is the neurons that manage movement that are damaged. A receptor on microglial cells, called TREM2, can clear a protein that builds up in the brains of patients with ALS.
The ability of astrocytes to simultaneously regulate and integrate synaptic plasticity of nearby synapses is important for facilitating cognitive flexibility, researchers in South Korea report. It is thought that lower cognitive flexibility in brain disorders such as autism, schizophrenia, and early stages of Alzheimer’s disease is caused by the reduced function of N-methyl-D-aspartate receptors (NMDARs). While NMDARs are important receptors for synaptic plasticity and are activated by a number of agonists and co-agonists, the source of one of the co-agonists, D-serine, has been controversial1.
Blood taken from young adult mice that get lots of exercise benefits the brains of same-aged, sedentary mice, new research1 shows. A single protein called clusterin in the blood of exercising mice seems mainly responsible for the effect. The finding could open the door to treatments that lower risk of neurodegenerative disease or slow its progression in people who don’t get much exercise by taming brain inflammation. Researchers found that transfusions of blood from running mice reduced neuroinflammation in the sedentary mice and improved their cognitive performance.
Nodes of Ranvier are myelin sheath gaps. They appear along a myelinated axon where the axolemma is exposed to the extracellular space. Nodes of Ranvier are uninsulated and highly enriched in ion channels, allowing them to participate in the exchange of ions required to regenerate the action potential. Nerve conduction in myelinated axons is referred to as saltatory conduction due to the manner in which the action potential seems to “jump” from one node to the next along the axon.
Substituting a single nucleotide in the gene coding for the nicotinic acetylcholine receptor can lead to functional changes in airway cells and result in symptoms similar to COPD, independent of smoking, new research1 has found. Chronic obstructive pulmonary disease (COPD) is a progressive chronic respiratory disease characterized by permanently obstructed airways. Symptoms include a chronic cough, sputum and breathing difficulties, which intensify over the course of several years and eventually become debilitating.
The process of packaging neurotransmitters may be responsible for the brain’s consumption of energy when its neurons are not active, researchers at Weill Cornell Medicine have found. Pound for pound, the brain consumes vastly more energy than other organs - using ~20% of the body’s fuel intake but making up only ~2 to 2.5% of it’s mass. Their study1 identifies tiny capsules called synaptic vesicles as a major source of energy consumption in inactive neurons.