Protein Linked to Learning also Induces Cocaine Addiction: Researchers

The study describes how the learning-related protein works with other proteins to forge new pathways in the brain in response to a drug-induced rush of the "pleasure" molecule dopamine.

By adding important detail to the process of addiction, the researchers, led by a group at Johns Hopkins, said that the work may point the way to new treatments.

"The broad question was why and how cocaine strengthened certain circuits in the brain long term, effectively re-wiring the brain for addiction," Paul Worley, M.D., a professor in the Solomon H. Snyder Department of Neuroscience at the Johns Hopkins University School of Medicine, said.

"What we found in this study was how two very different types of systems in the brain work together to make that happen," he said.

The study is published in the journal Cell.

Source-ANI

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Alzheimer's Disease Protein Controls Movement in Mice: Researchers

Alzheimer's disease is the most common form of dementia found in older adults. The World Health Organization estimates that approximately 18 million people worldwide have Alzheimer's disease. The number of people affected by the disease may increase to 34 million by 2025. Scientists know that the protein beta-secretase-1 or Bace1, a protease enzyme that breaks down proteins into smaller molecules, is involved in Alzheimer's disease. Bace1 cleaves the amyloid precursor protein and generates the damaging Abeta peptides that accumulate as plaques in the brain leading to disease. Now scientists have revealed in more detail how Bace1 works.

"Our results show that mice that lack Bace1 proteins or are treated with inhibitors of the enzyme have difficulties in coordination and walking and also show reduced muscle strength," remarked Carmen Birchmeier, one of the authors of the paper, Professor at the Max-Delbr?ck-Center for Molecular Medicine in Berlin, Germany, and an EMBO Member. "In addition, we were able to show that the combined activities of Bace1 and another protein, neuregulin-1 or Nrg1, are needed to sustain the muscle spindles in mice and to maintain motor coordination."

Muscle spindles are sensory organs that are found throughout the muscles of vertebrates. They are able to detect how muscles stretch and convey the perception of body position to the brain. The researchers used genetic analyses, biochemical studies and interference with pharmacological inhibitors to investigate how Bace1 works in mice. "If the signal strength of a specific form of neuregulin-1 known as IgNrg1 is gradually reduced, increasingly severe defects in the formation and maturation of muscle spindles are observed in mice. Furthermore, it appears that Bace1 is required for full IgNrg1 activity. The graded loss of IgNrg1 activity results in the animals having increasing difficulties with movement and coordination," says Cyril Cheret, the first author of the work.

Drug developers are interested in stopping the Bace1 protein in its tracks because it represents a promising route to treat Alzheimer's disease. If the protein were inhibited, it would interfere with the generation of the smaller damaging proteins that accumulate in the brain as amyloid plaques and would therefore provide some level of protection from the effects of the disease. "Our data indicate that one unwanted side effect of the long-term inhibition of Bace1 might be the disruption of muscle spindle formation and impairment of movement. This finding is relevant to scientists looking for ways to develop drugs that target the Bace1 protein and should be considered," says Birchmeier. Several Bace1 inhibitors are currently being tested in phase II and phase III clinical trials for the treatment of Alzheimer's disease.

Source-Eurekalert

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Newly Identified Immune Protein Could Stop Diabetes in Its Tracks: Melbourne Researchers

The discovery has wider repercussions, as the protein is responsible for protecting the body against excessive immune responses, and could be used to treat, or even prevent, other immune disorders such as multiple sclerosis and rheumatoid arthritis.

Professor Len Harrison, Dr Esther Bandala-Sanchez and Dr Yuxia Zhang led the research team from the Walter and Eliza Hall Institute's Molecular Medicine division that identified the immune protein CD52 as responsible for suppressing the immune response, and its potential for protecting against autoimmune diseases.

So-called autoimmune diseases develop when the immune system goes awry and attacks the body's own tissues. Professor Harrison said CD52 held great promise as a therapeutic agent for preventing and treating autoimmune diseases such as type 1 diabetes.

"Immune suppression by CD52 is a previously undiscovered mechanism that the body uses to regulate itself, and protect itself against excessive or damaging immune responses," Professor Harrison said.

"We are excited about the prospect of developing this discovery to clinical trials as soon as possible, to see if CD52 can be used to prevent and treat type 1 diabetes and other autoimmune diseases. This has already elicited interest from pharmaceutical companies," he noted.

Type 1 diabetes is an autoimmune disease that develops when immune cells attack and destroy insulin-producing beta cells in the pancreas.

Professor Harrison said that T cells that have or release high levels of CD52 are necessary to maintain normal balance in the immune system.

"In a preclinical model of type 1 diabetes, we showed that removal of CD52-producing immune cells led to rapid development of diabetes. We think that cells that release CD52 are essential to prevent the development of autoiummune disease, and that CD52 has great potential as a therapeutic agent," he said.

CD52 appears to play a dominant role in controlling or suppressing immune activity in the early stages of the immune response, Professor Harrison said.

"We identified a specialised population of immune cells (T cells) that carry high levels of CD52, which they release to dampen the activity of other T cells and prevent uncontrolled immune responses," Professor Harrison said.

"The cells act as an early 'braking' mechanism," he added.

Professor Harrison said his goal is to prevent and ultimately cure type 1 diabetes.

He revealed that they can prevent and cure type 1 diabetes in animal models and he's hopeful that these results will be translatable into humans, hopefully in the not-too-distant future.

The research was published today in the journal Nature Immunology.

Source-ANI

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High Protein Diet May Not be Very Effective in Reducing Body Weight and Risk of Heart Disease

The recent study published in the BioMed Central Nutrition Journal, aimed at identifying the long-term benefits of low protein diet and high protein diet in reducing body weight and risk of heart disease.

Researchers systematically reviewed 15 long term randomized control studies that compared low and high protein diets, low in fat, and estimated the dietary effects on weight, waist circumference, fat mass, total body cholesterol, LDL and HDL cholesterol, triacylglycerols, blood pressure, C-reactive protein (CRP), fasting glucose, fasting insulin and glycosylated hemoglobin.

Primary analysis of the findings revealed that a decrease in fasting insulin and an increase in good cholesterol (LDL cholesterol) were significant with high protein diets. However, with further analysis, the increase in HDL levels was attributed to the high fat content in the diet rather than the protein content.

The analysts note that the findings of the studies do not reveal any significant benefits of high protein diet on the biomarkers for obesity, heart disease and blood sugar level.

Hence, the authors opine that further research is required before high protein diets are recommended as a control measure for obesity and heart disease.

Reference:

Long-term effects of low-fat diets either low or high in protein on cardiovascular and metabolic risk factors: a systematic review and meta-analysis; Lukas et al; BMC Nutrition Journal 2013.

Source-Medindia

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