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Disease Modifying Therapies (disease + modifying_therapy)
Selected AbstractsDisease modifying therapy for AD?,JOURNAL OF NEUROCHEMISTRY, Issue 3 2006Todd E. Golde Alzheimer's disease (AD) is the most common form of dementia in industrialized nations. If more effective therapies are not developed that either prevent AD or block progression of the disease in its very early stages, the economic and societal cost of caring for AD patients will be devastating. Only two types of drugs are currently approved for the treatment of AD: inhibitors of acetyl cholinesterase, which symptomatically enhance cognitive state to some degree but are not disease modifying; and the adamantane derivative, memantine. Memantine preferentially blocks excessive NMDA receptor activity without disrupting normal receptor activity and is thought to be a neuroprotective agent that blocks excitotoxicty. Memantine therefore may have a potentially disease modifying effect in multiple neurodegenerative conditions. An improved understanding of the pathogeneses of AD has now led to the identification of numerous therapeutic targets designed to alter amyloid , protein (A,) or tau accumulation. Therapies that alter A, and tau through these various targets are likely to have significant disease modifying effects. Many of these targets have been validated in proof of concept studies in preclinical animal models, and some potentially disease modifying therapies targeting A, or tau are being tested in the clinic. This review will highlight both the promise of and the obstacles to developing such disease modifying AD therapies. [source] Translational medicine perspective in development of disease modifying therapies for Alzheimer's disease: biomarkers to buy down the riskDRUG DEVELOPMENT RESEARCH, Issue 2 2009Hong I. Wan Abstract Alzheimer's disease (AD) is a progressive neurodegenerative disease and the most common cause of age-related dementia. Currently available pharmacologic therapies, including acetylcholinesterase (AChE) inhibitors and N-methyl-D-aspartate (NMDA) receptor antagonists, only treat symptoms and do not address the underlying neurodegeneration. In addition to potentially improve the accuracy of diagnosis, biomarkers serve important roles for the development of putative disease-modifying drugs for AD. In this article, we review the existing and emerging areas of biomarker research and development for AD. Biochemical biomarkers in cerebrospinal fluid have been used to provide a link to disease pathology and may provide important proof of concept data for several classes of emerging therapeutics. Imaging biomarkers including volumetric magnetic resonance imaging and positron emission tomography assessing either glucose utilization or radioligands binding to amyloid plaque are discussed. Appropriate uses of these biomarkers in the context of the development of disease-modifying therapies are discussed. Drug Dev Res 70, 2009. © 2009 Wiley-Liss, Inc. [source] Disease modifying therapy for AD?,JOURNAL OF NEUROCHEMISTRY, Issue 3 2006Todd E. Golde Alzheimer's disease (AD) is the most common form of dementia in industrialized nations. If more effective therapies are not developed that either prevent AD or block progression of the disease in its very early stages, the economic and societal cost of caring for AD patients will be devastating. Only two types of drugs are currently approved for the treatment of AD: inhibitors of acetyl cholinesterase, which symptomatically enhance cognitive state to some degree but are not disease modifying; and the adamantane derivative, memantine. Memantine preferentially blocks excessive NMDA receptor activity without disrupting normal receptor activity and is thought to be a neuroprotective agent that blocks excitotoxicty. Memantine therefore may have a potentially disease modifying effect in multiple neurodegenerative conditions. An improved understanding of the pathogeneses of AD has now led to the identification of numerous therapeutic targets designed to alter amyloid , protein (A,) or tau accumulation. Therapies that alter A, and tau through these various targets are likely to have significant disease modifying effects. Many of these targets have been validated in proof of concept studies in preclinical animal models, and some potentially disease modifying therapies targeting A, or tau are being tested in the clinic. This review will highlight both the promise of and the obstacles to developing such disease modifying AD therapies. [source] Should neurologists wait and see or see and treat RRMS?PROGRESS IN NEUROLOGY AND PSYCHIATRY, Issue 5 2009David Bates MA Early and aggressive treatment of rheumatoid arthritis (RA) is now regarded as best practice to limit irreversible joint damage. However, in the case of relapsing remitting multiple sclerosis (RRMS), current guidelines recommend that disease modifying therapy should only be initiated in patients with evidence of actively progressing disease. Here, the authors present the key findings of the Programme Identifying and Observing Novel Therapy Adoption in Chronic Diseases (PIONEER) study to examine the reasons for these different management approaches. Copyright © 2009 Wiley Interface Ltd [source] Optic neuritis and multiple sclerosisACTA OPHTHALMOLOGICA, Issue 3 2001Mats Söderström ABSTRACT. Purpose: Review of the association between optic neuritis (ON) and multiple sclerosis (MS). Results: MS often presents as acute unilateral ON. While it is clear that many patients with ON suffer from a generalized disease of the central nervous system that will go on to clinically definite MS (CDMS), it is also clear that others do not. With more and more well-informed patients and the emerging pharmacotheraphy for MS, the distinction between those patients with ON who have MS and those who do not, has become more important than ever before. Recently, a large randomized clinical trial on patients with ON or other clinically isolated syndromes suggestive of MS and evidence of prior subclinical demyelination on magnetic resonance imaging of the brain, found that treatment with recombinant interferon-beta-1a is beneficial by reducing the development of CDMS. Conclusion: Ophthalmologists should refer their patients with acute ON to a neurologist for MS-directed investigations and decisions regarding early institution of disease modifying therapy. [source] | ||||||||||