Design and Analysis for Demonstrating Disease Modification Effects

2012 ◽  
pp. 405-408
Author(s):  
Djokouri Kouassi ◽  
Annpey Pong
Keyword(s):  
Disease Modification

scholarly journals The Role of Statins in Disease Modification and Cardiovascular Risk in Rheumatoid Arthritis

2018 ◽  
Vol 5 ◽  
Author(s):  
Stergios Soulaidopoulos ◽  
Elena Nikiphorou ◽  
Theodoros Dimitroulas ◽  
George D. Kitas
Keyword(s):  
Rheumatoid Arthritis ◽  
Cardiovascular Risk ◽  
Disease Modification

scholarly journals Antiepileptogenesis and disease modification: Clinical and Regulatory Issues

2021 ◽  
Author(s):  
Jacqueline A. French ◽  
Martina Bebin ◽  
Marc A. Dichter ◽  
Jerome Engel ◽  
Adam L. Hartman ◽  
...  
Keyword(s):  
Disease Modification ◽  
Regulatory Issues

Measuring Disease Modification in Alzheimer's Disease

CNS Spectrums ◽  
2007 ◽  
Vol 12 (S1) ◽  
pp. 11-14
Author(s):  
Jeffrey L. Cummings
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Immunoglobulin A ◽  
Disease Process ◽  
Underlying Disease ◽  
Therapeutic Interventions ◽  
Disease Modification ◽  
Amyloid Disease ◽  
Therapeutic Modalities ◽  
Disease Modifying

AbstractWe appear to be on the brink of a new epoch of treatment for Alzheimer's disease. Compelling evidence suggests that Aβ42 secretion is the triggering event in the pathogenesis of Alzheimer's disease, and that tau aggregation may be an important secondary event linked to neurodegeneration. Prophylactic administration of anti-amyloid agents designed to prevent Aβ accumulation in persons with subclinical disease is likely to be more effective than therapeutic interventions in established Alzheimer's disease. Drug development programs in Alzheimer's disease focus primarily on agents with anti-amyloid disease-modifying properties, and many different pharmacologic approaches to reducing amyloid pathology and tauopathy are being studied. Classes of therapeutic modalities currently in advanced-stage clinical trial testing include forms of immunotherapy (active β -amyloid immunoconjugate and human intravenous immunoglobulin), a γ-secretase inhibitor, the selective Aβ42-lowering agent R-flurbiprofen, and the anti-aggregation agent tramiprosate. Non-traditional dementia therapies such as the HMG-CoA reductase inhibitors (statins), valproate, and lithium are now being assessed for clinical benefit as anti-amyloid disease-modifying treatments. Positive findings of efficacy and safety from clinical studies are necessary but not sufficient to demonstrate that a drug has disease-modifying properties. Definitive proof of disease-modification requires evidence from validated animal models of Alzheimer's disease; rigorously controlled clinical trials showing a significantly improved, stabilized, or slowed rate of decline in cognitive and global function compared to placebo; and prospectively obtained evidence from surrogate biomarkers that the treatment resulted in measurable biological changes associated with the underlying disease process.

Evaluation of electroacupuncture for symptom modification in a rodent model of spontaneous osteoarthritis

2021 ◽  
pp. 096452842110207
Author(s):  
Alexa P Spittler ◽  
Maryam F Afzali ◽  
Richard B Martinez ◽  
Lauren A Culver ◽  
Sarah E Leavell ◽  
...  
Keyword(s):  
Rodent Model ◽  
Knee Joints ◽  
Control Group ◽  
Disease Modification ◽  
Inflammatory Biomarker ◽  
Knee Oa ◽  
Significant Difference ◽  
Gene Transcripts ◽  
Restricted Mobility ◽  
Movement Parameters

Objective: Faced with the frustration of chronic discomfort and restricted mobility due to osteoarthritis (OA), many individuals have turned to acupuncture for relief. However, the efficacy of acupuncture for OA is uncertain, as much of the evidence is inconclusive. The purpose of this study was to evaluate electroacupuncture (EA) in a rodent model of OA such that conclusions regarding its effectiveness for symptom or disease modification could be drawn. Methods: Ten 12-month-old male Hartley guinea pigs—which characteristically have moderate to advanced OA at this age—were randomly assigned to receive EA for knee OA (n = 5) or anesthesia only (control group, n = 5). Treatments were performed three times weekly for 3 weeks, followed by euthanasia 2 weeks later. Gait analysis and enclosure monitoring were performed weekly to evaluate changes in movement. Serum was collected for inflammatory biomarker testing. Knee joints were collected for histology and gene expression. Results: Animals receiving EA had significantly greater changes in movement parameters compared to those receiving anesthesia only. There was a tendency toward decreased serum protein concentrations of complement component 3 (C3) in the EA group compared to the control group. Structural and antioxidant gene transcripts in articular cartilage were increased by EA. There was no significant difference in total joint histology scores between groups. Conclusion: This study provides evidence that EA has a positive effect on symptom, but not disease, modification in a rodent model of OA. Further investigations into mechanistic pathways that may explain the efficacy of EA in this animal model are needed.

scholarly journals Disease modification in partial epilepsy

Brain ◽  
2002 ◽  
Vol 125 (9) ◽  
pp. 1937-1950 ◽  
Author(s):  
M. C. Walker
Keyword(s):  
Partial Epilepsy ◽  
Disease Modification
Sign in / Sign up

Export Citation Format

Share Document