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星期五, 18. 五月 2012

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September 2011
IS BIOMARKER DISCOVERY IN PSYCHIATRIC DISORDERS BEING INHIBITED BY A LACK OF STANDARDISED PROTOCOLS AND CURRENT DIAGNOSTIC CRITERIA? As in many areas of medicine there is a growing effort to identify useful biomarkers to aid the diagnoses and treatment of psychiatric disorders. Attempts are being made to discover biomarkers that may delineate psychiatric disorders according to existing diagnostic criteria, to delineate sub-groups within existing syndrome level diagnostic criteria such as schizophrenia or to discover intermediate phenotypes within such diagnoses. In addition, biomarkers are been sort to provide some biological measure of treatment responsiveness in people with psychiatric disorders. Experience with disorders such as diabetes1 suggest this will be a long and involved undertaking and it must be questioned as to whether current efforts in psychiatry are being built on solid enough foundations to ensure successful outcomes.
June 2011
Clinical trials of amyloid-targeting compounds in Alzheimer’s disease For more than a century, accumulation of fibrillar amyloid beta (Aβ) plaques in the brain has been established as one of the most prominent pathological hallmarks of AD. Based on numerous subsequent findings from in vitro experiments and in vivo animal models showing that specific forms of Aβ peptides have synaptotoxic and neurotoxic properties, a major pathogenetic role of Aβ in AD has been proposed, resulting in the so called amyloid-cascade hypothesis. This concept proposes various downstream pathological changes, which are thought to be initiated by toxic levels of Aβ levels and which include formation of neurofbrillary tangles (NFTs), neuro-inflammatory events, destruction of synapses, dendrites and axons, apoptotic neuronal cell death, brain atrophy and ultimately clinical dementia syndrome (Hardy & Allsop, 1991). Another supporting evidence for a major causative role of Aβ-metabolism in AD came from the finding that autosomal dominant forms of early-onset AD (ADAD) are mostly based on mutations in genes which encode for the amyloid precursor protein (APP) or for the presenilin proteins (PSEN1/PSEN2), all of which are critically involved in the generation of Aβ. Similarly, animal models harbouring human APP mutations show age-dependent accumulation of Aβ in the brain and cognitive deficits (Higgins & Jacobsen, 2003).
March 2011
IS THE EFFICACY OF ANTIDEPRESSANTS CLINICALLY RELEVANT? At first glance the title of this statement will seem astonishing to most clinicians, since their clinical experience (Möller 2009) reassures them every day of the clinically relevant efficacy of antidepressants. However, in times of evidence-based medicine and pharmacoeconomics, clinicians have to adapt to a situation in which such common grounds are investigated predominantly by people from outside their own professional community - for example, by evidence-based medicine (EBM) researchers or health economists.