Tag Archives: mice

Female and male hearts respond differently to stress hormone in mouse study

A new study published in Science Advances shows female and male hearts respond differently to the stress hormone noradrenaline. The study in mice may have implications for human heart disorders like arrhythmias and heart failure and how different sexes respond to medications.

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The team built a new type of fluorescence imaging system that allows them to use light to see how a mouse heart responds to hormones and neurotransmitters in real time. The mice were exposed to noradrenaline, also known as norepinephrine. Noradrenaline is both a neurotransmitter and hormone associated with the body’s “fight or flight” response.

The results reveal that male and female mouse hearts respond uniformly at first after exposure to noradrenaline. However, some areas of the female heart return to normal more quickly than the male heart, which produces differences in the heart’s electrical activity.

“The differences in electrical activity that we observed are called repolarization in the female hearts. Repolarization refers to how the heart resets between each heartbeat and is closely linked to some types of arrhythmias,” said Jessica L. Caldwell, first author of the study. Caldwell is a postdoctoral scholar in the UC Davis School of Medicine Department of Pharmacology.

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Exercise increases dopamine release in mice

Exercise increases dopamine signaling in the motor areas of mice, according to research recently published in JNeurosci.

It’s no secret exercise is good for the brain — working out can improve mood, sharpen memory, and stave off cognitive decline. Exercise even improves motor behavior in people with Parkinson’s disease, but the exact mechanism is not known. One possibility is through an increase in dopamine, a neurotransmitter needed for motor and emotional control that declines as the disease progresses.

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Bastioli et al. compared dopamine signaling in mice after 30 days of voluntary wheel running or inactivity. In the runner mice, dopamine release in the striatum (a motor area) increased in response to electrical stimulation, while there was no change in sedentary mice. The increased dopamine release remained even a week after the exercise ended. The researchers also measured increased levels of brain-derived neurotrophic factor (BDNF), a protein involved in neuron health, in the striatum of active mice. When the researchers repeated the experiments in a genetic mouse model lacking BDNF, there was no difference in dopamine release between the active and sedentary mice, suggesting BDNF catalyzes increased dopamine signaling. Future studies will examine if the relationship holds true in a mouse model of Parkinson’s disease, and if exercise can improve motor outcomes. 

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Experimental drug shows potential against Alzheimer’s disease

Researchers have designed an experimental drug that reversed key symptoms of Alzheimer’s disease in mice. The drug works by reinvigorating a cellular cleaning mechanism that gets rid of unwanted proteins by digesting and recycling them.

Researchers at Albert Einstein College of Medicine have designed an experimental drug that reversed key symptoms of Alzheimer’s disease in mice. The drug works by reinvigorating a cellular cleaning mechanism that gets rid of unwanted proteins by digesting and recycling them. The study was published online today in the journal Cell.

“Discoveries in mice don’t always translate to humans, especially in Alzheimer’s disease,” said co-study leader Ana Maria Cuervo, M.D., Ph.D., the Robert and Renée Belfer Chair for the Study of Neurodegenerative Diseases, professor of developmental and molecular biology, and co-director of the Institute for Aging Research at Einstein. “But we were encouraged to find in our study that the drop-off in cellular cleaning that contributes to Alzheimer’s in mice also occurs in people with the disease, suggesting that our drug may also work in humans.” In the 1990s, Dr. Cuervo discovered the existence of this cell-cleaning process, known as chaperone-mediated autophagy (CMA) and has published 200 papers on its role in health and disease.

CMA becomes less efficient as people age, increasing the risk that unwanted proteins will accumulate into insoluble clumps that damage cells. In fact, Alzheimer’s and all other neurodegenerative diseases are characterized by the presence of toxic protein aggregates in patients’ brains. The Cell paper reveals a dynamic interplay between CMA and Alzheimer’s disease, with loss of CMA in neurons contributing to Alzheimer’s and vice versa. The findings suggest that drugs for revving up CMA may offer hope for treating neurodegenerative diseases.

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Mouse anti-aging compound improves muscle glucose metabolism in people

A natural compound previously demonstrated to counteract aspects of aging and improve metabolic health in mice has clinically relevant effects in people, according to new research at Washington University School of Medicine in St. Louis.

A small clinical trial of postmenopausal women with prediabetes shows that the compound NMN (nicotinamide mononucleotide) improved the ability of insulin to increase glucose uptake in skeletal muscle, which often is abnormal in people with obesity, prediabetes or Type 2 diabetes. NMN also improved expression of genes that are involved in muscle structure and remodeling. However, the treatment did not lower blood glucose or blood pressure, improve blood lipid profile, increase insulin sensitivity in the liver, reduce fat in the liver or decrease circulating markers of inflammation as seen in mice.

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The study, published online April 22 in the journal Science, is the first randomized clinical trial to look at the metabolic effects of NMN administration in people.

Among the women in the study, 13 received 250 mg of NMN orally every day for 10 weeks, and 12 were given an inactive placebo every day over the same period.

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