The most usual case of dementia is Alzheimer’s disease. The expression dementia designates a lot of symptoms that can include memory loss and difficulties with thinking, problem-solving or oral communication. These symptoms happen when the brain is damaged by certain diseases, including Alzheimer’s disease. During this condition, proteins build up in the brain to form structures called ‘plaques’ and ‘tangles’, which contributes to the loss of connections between nerve cells, and eventually to the destruction of nerve cells and loss of brain tissue.
A lot of the research examining the causes of dementia has focused on Apolipoprotein E (ApoE), which in certain genetic forms can support the buildup of toxic amyloid plaques in the brains of Alzheimer’s patients. Researchers at the Institute’s Center for Translational Neurodegeneration Research and elsewhere are trying to determine whether reducing ApoE in the brain could finally be a feasible therapeutic alternative for treating Alzheimer’s.
The retrospective study examines how various bodily systems fail due to ApoE, which, among other functions is responsible for transporting and filtering b-amyloid, the toxic substance that accumulates in Alzheimer’s disease.
The type of ApoE produced by the ApoE gene determines how effectively amyloid is removed from the brain. ApoE2 is the most effective, ApoE3 is in the middle and ApoE4 is the least efficient and therefore most likely to allow the buildup of amyloid plaques. People whose genes produce ApoE4 are at high hazard of getting Alzheimer’s, according to the review compiled by Center Director Dr. Joachim Herz, Professor of Molecular Genetics, Neuroscience, and Neurology and Neurotherapeutics, and Courtney Lane-Donovan, a Medical Science Training Program student.
Neurodevelopmental disorders are linked up with widely varying points of difficulty which may have substantial mental, emotional, physical, and economic consequences for individuals, and in turn their families and social club in general. Autism spectrum disorder is found to be one of the challenging conditions, in which the specific cause is yet to be found. The wellness of the mother during pregnancy takes on a major part in the growth of the fetus. It is natural that our immune system defend us against foreign invaders. In the case of pregnancy, the maternal immune activation sometimes leads to the risk of autism and prenatal brain development.
In a recent study, researchers at the University of Cyprus, University of California, University of Cambridge, San Diego and Stanford University used rodents to help represent the complex biological cascade caused by the mother’s immune response, which may lead to important consequences. They stated that,”It’s important to underline that the increment in risk is genuinely small – too low to be meaningfully applied to specific individuals, and is exclusively seen in very large studies when examining many thousands of people”. For understanding how activation of a mother’s immune system may bear on her child’s brain development, the researchers analyzed the natural action of genes in the brain after injecting pregnant rats and mice with a substance called lipopolysaccharide. There’s no infectious agent in this substance and thus does not make the mothers sick, but will elicit a potent immune response in the mother, characterized by an increase in levels of cytokines. These are small immune signalling molecules that can have significant effects on brain cells and the associations between these cells.
The scientists found that maternal immune activation alters the action of multiple genes and pathways in the fetus’s brain. Significantly, many of these genes are recognized to be significant in the development of autism and to key brain developmental processes that happen before birth. They think that these effects may help to explain why maternal immune activation carries a modest increased risk for later atypical neurodevelopment. While the effects induced by maternal immune activation are transient, the researchers indicate that they may be very potent during fetal development and may cause different characteristics in the individual depending on when it occurs during gestation. The study emphasizes the importance of the idea that genes and the environment interact and that their interaction may have important roles in better understanding how risk for neurodevelopmental disorder manifests.
Be it sleeping, eating or working – a mood disorder is the toughest thing that will affect all your everyday actions. Your thoughts hold a mysterious connection with depression. You can get rid yourself of depression by learning to master your thoughts. All you require to know is your thought does not bounce back reality.
Are you a person with depression? There’s no need to worry and ruminate anymore.
A new research carried out by NTNU researchers, Department of Psychology, shows that learning how to ruminate less on thoughts and emotions has given a positive effect for people with depression.
Researchers at NTNU’s Department of psychology, has recently issued a scientific paper on the treatment of depression using Metacognitive therapy (MCT). The patient involved in this study was treated over a period of ten weeks. After six months, 80 percent of them had reached full recovery from their depression diagnosis. Too, the follow-up after six months revealed the same tendency. During the study, the team tries to ascertain out how the patient’s mood and thinking process work. This therapy addresses the thinking process and focuses on lessening the ruminating process. By becoming conscious of what occurs when they start to ruminate, patient gains to control their thoughts. The comparison of MCT group and the one that did not receive treatment strengthened the result of this study. Professor Roger Hagen in NTNU’s Department of Psychology says, Hope that Metacognitive Therapy will become the most common way to treat depression in Norway.
Most of the young people and athletes facing unexpected death due to sudden cardiac arrest. One of the rare genetic disorders, Arrhythmogenic Right Ventricle Cardiomyopathy (ARVC) is found to be the one that inclined the patient’s to cardiac arrest.
An international collaborative research led by the researchers in Canada, South Africa and Italy has successfully identified a novel gene – CDH2, which is responsible for ARVC that leads to sudden death amongst young people and athletes. The study was carried out by a South African team headed by Bongani Mayosi, a professor of cardiology at the University of Cape Town and Groote Schuur Hospital, along with researchers of the Italian Auxologico Institute of Milan and the University of Pavia. The genetic sequencing and the bioinformatics analysis for this study were done by a team of investigators from the Population Health Research Institute of McMaster University and Hamilton Health Sciences, led by Dr. Guillaume Pare.
Bongani Mayosi monitored a South African family for 20 years. They were affected by ARVC that had experienced several cases of young sudden death. The Italian researchers sequenced all the coding regions of the genome in two ailing members of the family, eliminating all genetic causes known at the time. The genetic mutation responsible for the disease in the family, CDH2, was narrowed down from more than 13,000 common genetic variants present in the two ill patients.
CDH2 is liable for the production of Cadherin 2 or N-Cadherin, a key protein for normal adhesion between the cardiac cells. They validated the gene’s discovery by finding a second mutation on the same gene in another patient with ARVC from a different family. Agreeing to their previous studies, it was known that genetically modified mice without this protein tend to have malignant ventricular arrhythmias and sudden death.
The researchers concluded identifying the gene is important in clarifying the genetic mechanisms underlying ARVC, and it also makes the early detection of ARVC possible in otherwise unsuspecting people. They stated, this study may lead to reduction of cases of sudden death in patients with the mutation.