Mental Health Research Institute

About: Mental Health Research Institute is a facility organization based out in Melbourne, Victoria, Australia. It is known for research contribution in the topics: Schizophrenia & Population. The organization has 1291 authors who have published 1656 publications receiving 86577 citations.

COMT val158met Genotype Affects µ-Opioid Neurotransmitter Responses to a Pain Stressor

Abstract: Responses to pain and other stressors are regulated by interactions between multiple brain areas and neurochemical systems. We examined the influence of a common functional genetic polymorphism affecting the metabolism of catecholamines on the modulation of responses to sustained pain in humans. Individuals homozygous for the met 158 allele of the catechol- O -methyltransferase (COMT) polymorphism ( val 158 met ) showed diminished regional μ-opioid system responses to pain compared with heterozygotes. These effects were accompanied by higher sensory and affective ratings of pain and a more negative internal affective state. Opposite effects were observed in val 158 homozygotes. The COMT val 158 met polymorphism thus influences the human experience of pain and may underlie interindividual differences in the adaptation and responses to pain and other stressful stimuli.

Imaging beta-amyloid burden in aging and dementia.

Abstract: I read the article by Rowe et al.1 with interest. Diagnosing Alzheimer disease (AD) in a preclinical phase would enable early implementation of therapeutic interventions which might have long-term benefits. PET technology by using the Pittsburgh compound (PiB) allows detection of amyloid deposits in the brain.1,2 Pathologic studies indicate that amyloid deposition is present in cortical regions of all patients with AD even before the onset of dementia.3 One application of PiB-PET may be all that is necessary to identify the neuropathologic changes of AD in clinically normal individuals prior to the development of cognitive changes. These individuals would be considered to have preclinical AD. PET studies performed with PiB in cognitively intact subjects have shown that between 15 and 22% of them had abnormal scans.1,2 The objective is to determine who and when someone will become demented. It is and will be unclear because the proportion of subjects with cerebral amyloid deposits is, and will be, higher than the proportion of people with clinical AD. Otherwise, it is impossible to understand pathologic observations which indicate that more than 30% of older persons over age 75 die without any clinical evidence of dementia despite showing amyloid deposits and pathologic changes characteristic of AD.3 Presumably all of them would have abnormal PiB-PET scans. Amyloid deposition is not synonymous with clinical AD unless we assume that everyone with an abnormal PiB-PET scan would develop AD. Even in this case, many of them (70% according to pathologic data and prevalence estimates of AD) will die without dementia in the …

A review on the oxidative and nitrosative stress (O&NS) pathways in major depression and their possible contribution to the (neuro)degenerative processes in that illness.

Abstract: This paper reviews the body of evidence that major depression is accompanied by a decreased antioxidant status and by induction of oxidative and nitrosative (ION and increased 8-hydroxy-2-deoxyguanosine, indicating oxidative DNA damage. There is also evidence in major depression, that ON and increased IgM-mediated immune responses against membrane fatty acids, like phosphatidyl inositol (Pi); oleic, palmitic, and myristic acid; and NO modified amino-acids, e.g. NO-tyrosine, NO-tryptophan and NO-arginine; and NO-albumin. There is a significant association between depression and polymorphisms in O&NS genes, like manganese superoxide dismutase, catalase, and myeloperoxidase. Animal models of depression very consistently show lowered antioxidant defences and activated O&NS pathways in the peripheral blood and the brain. In animal models of depression, antidepressants consistently increase lowered antioxidant levels and normalize the damage caused by O&NS processes. Antioxidants, such as N-acetyl-cysteine, compounds that mimic GPX activity, and zinc exhibit antidepressive effects. This paper reviews the pathways by which lowered antioxidants and O&NS may contribute to depression, and the (neuro)degenerative processes that accompany that illness. It is concluded that aberrations in O&NS pathways are--together with the inflammatory processes--key components of depression. All in all, the results suggest that depression belongs to the spectrum of (neuro)degenerative disorders.