Sentences with phrase «human brain diseases in»

The massive number of cells within the OSVZ of humans «tells us we have to be careful when modeling human brain diseases in mice,» says Kriegstein.

Not exact matches

According to the University of Maryland Medical Center polyunsaturated fatty acids (PUFAs)-- also known as omega - 3 fatty acids — play a crucial role in human brain function, as well as normal growth and development, with research showing that they can also reduce inflammation in addition to helping lower the risk of chronic diseases such as heart disease, cancer, and arthritis.

Studies have shown that a protein in human milk aids in brain development, and breast - fed babies are less likely to get gastrointestinal infections and diarrhea, respiratory and ear infections or more serious diseases such as pneumonia, and there is a lower risk of Sudden Infant Death Syndrome.

«We don't know if the observed reversibility of the disease symptoms as observed in the mouse,» he says, «exists in humans who have a much longer period of pre - and post-natal brain development than mice — months and years in humans, weeks in mice.»

Since the first human brain organoids were created from stem cells in 2013, scientists have gotten them to form structures like those in the brains of fetuses, to sprout dozens of different kinds of brain cells, and to develop abnormalities like those causing neurological diseases such as Timothy syndrome.

Gene therapy delivered to a specific part of the brain reverses symptoms of depression in a mouse model of the disease — potentially laying the groundwork for a new approach to treating severe cases of human depression in which drugs are ineffective.

Degenerative brain diseases like mad cow disease (officially known as bovine spongiform encephalopathy, or BSE), scrapie in sheep, and vCJD in humans are thought to be caused by prions, misfolded versions of a normal cellular protein called PrPC.

The behavioral tests used here modeled one dimension of the disease — an inability to experience pleasure from normal activities — but not others, such as stress and anxiety, and probably tap into different brain mechanisms in mice than in humans, he says.

The results, published online in the journal Brain, Behavior and Immunity, strengthen the case that transgenic Huntington's disease monkeys could be used to evaluate emerging treatments (such as this) before launching human clinical trials.

To investigate, Walker Jackson of the Whitehead Institute in Boston, Massachusetts, and his colleagues created mice with a mutation associated with the human prion disease Fatal Familial Insomnia and injected some of their brain tissue into the brains of mice without the mutation.

A genetic mutation protecting against kuru — a brain disease passed on by eating human brains — only emerged and spread in the past 200 years.

The findings, appearing online Feb. 19, 2015, in Current Biology, may lend insight into not only what makes the human brain special but also why people get some diseases, such as autism and Alzheimer's disease, whereas chimpanzees don't.

In humans, Huntington's is an inherited disease caused by a gene encoding a toxic protein, called mutant huntingtin, which causes brain cells to die.

A recent study published in Annals of Neurology reports that healthy human tissue grafted to the brains of patients with Huntington's disease in the hopes of treating the neurological disorder also developed signs of the illness, several years after the graft.

An inflammatory protein that triggers a pregnant mouse's immune response to an infection or other disease appears to cause brain injury in her fetus, but not the premature birth that was long believed to be linked with such neurologic damage in both rodents and humans, new Johns Hopkins - led research suggests.

The newly identified gene affects accumulation of amyloid - beta, a protein believed to be one of the main causes of the damage that underpins this brain disease in humans.

Just as it does in dogs and humans, the disease attacks a wolf's brain, causing aggressive behavior and, eventually, death.

Svendsen is more optimistic about his team's work involving human tests of a novel stem cell approach to treat ALS, a degenerative motor neuron disease in which cells that transmit messages from the brain and spinal cord to the muscles wither or die.

The loss of a single gene in mice can affect social behavior and impair their brains» ability to filter out distractions — both characteristics of several neurological diseases in humans.

Her work is used in the assessment and detection of functional and anatomical change in the human brain through the course of Alzheimer's disease.

To maintain its foothold in large - scale, world - class research, Japan has launched its own Brain Mapping by Integrated Neurotechnologies for Disease Studies (Brain / MINDS) project, in line with the increasing interest in brain - mapping projects around the world, such as the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative project in the United States and the Human Brain Project (HBP) in EuBrain Mapping by Integrated Neurotechnologies for Disease Studies (Brain / MINDS) project, in line with the increasing interest in brain - mapping projects around the world, such as the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative project in the United States and the Human Brain Project (HBP) in EuBrain Mapping by Integrated Neurotechnologies for Disease Studies (Brain / MINDS) project, in line with the increasing interest in brain - mapping projects around the world, such as the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative project in the United States and the Human Brain Project (HBP) in EuBrain / MINDS) project, in line with the increasing interest in brain - mapping projects around the world, such as the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative project in the United States and the Human Brain Project (HBP) in EuBrain / MINDS) project, in line with the increasing interest in brain - mapping projects around the world, such as the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative project in the United States and the Human Brain Project (HBP) in Eubrain - mapping projects around the world, such as the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative project in the United States and the Human Brain Project (HBP) in Eubrain - mapping projects around the world, such as the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative project in the United States and the Human Brain Project (HBP) in EuBrain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative project in the United States and the Human Brain Project (HBP) in EuBrain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative project in the United States and the Human Brain Project (HBP) in EuBRAIN) Initiative project in the United States and the Human Brain Project (HBP) in EuBRAIN) Initiative project in the United States and the Human Brain Project (HBP) in EuBrain Project (HBP) in EuBrain Project (HBP) in Europe.

Future studies may reveal if changes in brain lactate are linked to neurodegenerative disease in humans, says Ross.

Several fatal neurological diseases — including Creutzfeldt - Jakob disease (CJD) in humans and scrapie in sheep — are marked by the accumulation of protein deposits in the brain.

They found that although the protein stayed soluble for a week or two, it eventually polymerized into long fibers resembling those in so - called prion diseases — brain diseases such as scrapie in sheep, «mad cow disease» in cattle, and Creutzfeldt - Jakob disease in humans.

Prion diseases originate when normally harmless prion protein molecules become abnormal and gather in clusters and filaments in the human body and brain.

Prions, whose normal function is unclear, are the likely cause of mad cow disease and similar brain disorders in animals and humans.

But recent studies in both humans and lab mice have suggested that motor neurons in the brain — the upper motor neurons — may be involved in disease progression, although the extent and significance of this involvement has remained unknown.

Since the current work was done in mice, O'Leary and Zembrzycki want to confirm the link in humans by using brain scans to measure the natural variation in the neocortical areas and search for potential links to disease.

«The imaging technique could shed light on the immune dysfunction that underpins a broad range of neuroinflammatory diseases, such as Alzheimer's disease, depression, post-traumatic stress disorder and addiction,» said Christine Sandiego, PhD, lead author of the study and a researcher from the department of psychiatry at the Yale School of Medicine in New Haven, Conn. «This is the first human study that accurately measures this immune response in the brain.

By pairing a receptor that targets neurons with a molecule that degrades the main component of Alzheimer's plaques, the biologists were able to substantially dissolve these plaques in mice brains and human brain tissue, offering a potential mechanism for treating the debilitating disease, as well as other conditions that involve either the brain or the eyes.

German and Canadian scientists have built a three dimensional map of the human brain to help in the development of new treatments for neurological disorders like Alzheimer's and Parkinson's disease.

«Using a technique developed by our collaborators at the University of Iowa, we were able to get long - term expression of these human gene variants in the fluid that bathes the entire brain,» says Bradley Hyman, MD, PhD, of the MassGeneral Institute for Neurodegenerative Disease (MGH - MIND), senior author of the report in the Nov. 20 Science Translational Medicine.

NIH gets an extra $ 414 million for Alzheimer's disease research, along with $ 400 million for the BRAIN Initiative, a research project announced by President Obama in 2013 that aims to improve our understanding of the human bBRAIN Initiative, a research project announced by President Obama in 2013 that aims to improve our understanding of the human brainbrain.

In a novel animal study design that mimicked human clinical trials, researchers at University of California, San Diego School of Medicine report that long - term treatment using a small molecule drug that reduces activity of the brain's stress circuitry significantly reduces Alzheimer's disease (AD) neuropathology and prevents onset of cognitive impairment in a mouse model of the neurodegenerative conditioIn a novel animal study design that mimicked human clinical trials, researchers at University of California, San Diego School of Medicine report that long - term treatment using a small molecule drug that reduces activity of the brain's stress circuitry significantly reduces Alzheimer's disease (AD) neuropathology and prevents onset of cognitive impairment in a mouse model of the neurodegenerative conditioin a mouse model of the neurodegenerative condition.

«It is possible that also in humans, inflammatory diseases that primarily develop outside the brain could trigger epigenetic reprogramming inside the brain,» says Neher.

Auriel Willette, a researcher in food science and human nutrition at Iowa State University, found evidence that an elevated presence of a protein called neuronal pentraxin - 2 may slow cognitive decline and reduce brain atrophy in people with Alzheimer's disease.

Suspecting that the disease works differently in humans, whose brains are much bigger and more complex than those of lab animals, Brivanlou, along with research associates Albert Ruzo and Gist Croft, developed a cell - based human system for their research.

The new study — published October 18, 2016 in the journal Molecular Psychiatry — combined genetic analysis of more than 9,000 human psychiatric patients with brain imaging, electrophysiology, and pharmacological experiments in mutant mice to suggest that mutations in the gene DIXDC1 may act as a general risk factor for psychiatric disease by interfering with the way the brain regulates connections between neurons.

Auriel Willette, a researcher in food science and human nutrition, found evidence that an elevated presence of a protein called neuronal pentraxin - 2 may slow cognitive decline and reduce brain atrophy in people with Alzheimer's disease.

At the Rockefeller meeting, an important impetus behind the big ambitions — the quest to decipher the gamut of human brain diseases that are still incredibly poorly understood — was evident in the room.

Researchers have discovered tell - tale signs of Alzheimer's disease in 20 elderly chimpanzee brains, rekindling a decades - old debate over whether humans are the only species that develop the debilitating condition.

By examining brain regions most affected by Alzheimer's disease pathology in humans, the group demonstrated that amyloid beta plaques and blood vessels were present in all 20 aged chimpanzee brains.

He added that the existence of episodic memory in lower animals has implications for research on human diseases that affect memory, including Alzheimer's, Parkinson's and Huntington's diseases, since the majority of research on the brain — and the drugs used to treat memory diseases and dementia — start out based on insights into how the brain works in rats.

Although genetically modified mice have been used widely to model neurodegenerative diseases, they lack the typical neurodegeneration or overt neuronal loss seen in human brains, says corresponding author Xiao - Jiang Li, MD, PhD, distinguished professor of human genetics at Emory University School of Medicine.

Humans are considered uniquely susceptible to Alzheimer's disease, potentially due to genetic differences, changes in brain structure and function during evolution, and an increased lifespan.

Researchers led by investigators Jerry Workman, Ph.D. and Susan Abmayr, Ph.D. at the Stowers Institute for Medical Research found that fruit flies that lack Ataxin - 7 experience neurodegeneration in the brain and the eye — paralleling the effects of the human disease.

«The presence of amyloid and tau pathology in aged chimpanzees indicates these Alzheimer's disease lesions are not specific to the human brain as generally believed,» Hof continued.

Extracts from the brains of FFI patients transmitted disease to transgenic mice expressing a chimeric human - mouse PrP gene about 200 days after inoculation and induced formation of the 19 - kilodalton PrPSc fragment, whereas extracts from the brains of familial and sporadic Creutzfeldt - Jakob disease patients produced the 21 - kilodalton PrPSc fragment in these mice.

Improvements on this scale happened in all the animals, including mice with a version of human Alzheimer's disease, elderly rats and monkeys with natural degeneration, plus rats and monkeys given brain lesions similar to those seen in Alzheimer's.

If the new mechanism also operates in the human brain and can be potentiated, this could become of clinical importance not only for stroke patients, but also for replacing neurons which have died, thus restoring function in patients with other disorders such as Parkinson's disease and Huntington's disease,» says Olle Lindvall, Senior Professor of Neurology.