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Journal articles on the topic 'Disease-modifying treatments'

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Published: 10 March 2023

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1

Galimberti, Daniela, and Elio Scarpini. "Disease-modifying treatments for Alzheimer’s disease." Therapeutic Advances in Neurological Disorders 4, no. 4 (April 20, 2011): 203–16. http://dx.doi.org/10.1177/1756285611404470.

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Waubant, Emmanuelle, Gavin Giovannoni, Chris Hawkes, and Michael Levy. "Vaccines and disease-modifying treatments." Multiple Sclerosis and Related Disorders 26 (November 2018): A1—A2. http://dx.doi.org/10.1016/j.msard.2018.10.017.

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3

Weilbach, Franz X., and Ralf Gold. "Disease Modifying Treatments for Multiple Sclerosis." CNS Drugs 11, no. 2 (1999): 133–57. http://dx.doi.org/10.2165/00023210-199911020-00005.

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4

Cummings, Jeffrey L. "Integrating Symptomatic- and Disease-Modifying Treatments." CNS Spectrums 13, S16 (2008): 28–30. http://dx.doi.org/10.1017/s1092852900027024.

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Although treatments for Alzheimer’s disease (AD) currently focus on symptomatic therapies, we are entering into an era of disease-modifying therapies. Central to disease modification is early diagnosis; the disease should be slowed as early as possible, maximizing the preservation of cognitive integrity. Ideally, AD should be diagnosed before the onset of dementia, perhaps with the use of biomarkers.Some therapies suggest that cholinesterase inhibitors and memantine have disease-modifying properties, though not all studies agree. Doody and colleagues have produced data suggesting that these agents may modify the course of AD, but it is not clear that they affect the underlying mechanisms that lead to cell death. Rather than being disease-modifying agents, cholinesterase inhibitors and memantine have potential as disease-course-modifying agents. Language precision will be extremely important in describing these therapies. One European consensus conference concluded that affecting disease course is not adequate for disease modification, but this has not been largely endorsed.Symptomatic therapies are those affecting the course of the disease. Their benefits are multidimensional, improving cognition, global assessment, activities of daily living, behavior, and caregiver burden. Symptomatic therapies should defer decline. Clinical trials show that symptomatic therapies produce an initial improvement above baseline. However, some patients experience observable changes and some experience none. These therapies are believed to produce ~1 point improvement on the Mini-Mental State Examination (MMSE) average, and a decline that is otherwise parallel to a placebo group after a period of delayed progression (Slide 1).

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Thomas, Emily, Brenda Wasunna‐Smith, and Tarun Kuruvilla. "Aducanumab and disease modifying treatments for Alzheimer's disease." Progress in Neurology and Psychiatry 25, no. 3 (July 2021): 4–6. http://dx.doi.org/10.1002/pnp.711.

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Roberts, S., J. Hendrick, A. Vinitsky, D. Barten, D. Izzarelli, M. Lewis, B. Robertson, et al. "Symptomatic and Disease Modifying Treatments of Alzheimer's Disease." CNS Drug Reviews 6 (June 7, 2006): 19. http://dx.doi.org/10.1111/j.1527-3458.2000.tb00168.x.

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7

Kieseier, Bernd C., and Heinz Wiendl. "Oral Disease-Modifying Treatments for Multiple Sclerosis." CNS Drugs 21, no. 6 (2007): 483–502. http://dx.doi.org/10.2165/00023210-200721060-00005.

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8

Comi, Giancarlo. "Disease-modifying treatments for progressive multiple sclerosis." Multiple Sclerosis Journal 19, no. 11 (September 23, 2013): 1428–36. http://dx.doi.org/10.1177/1352458513502572.

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The last 20 years have seen major progress in the treatment of relapsing–remitting multiple sclerosis (RRMS) using a variety of drugs targeting immune dysfunction. In contrast, all clinical trials of such agents in primary progressive multiple sclerosis (PPMS) have failed and there is limited evidence of their efficacy in secondary progressive disease. Evolving concepts of the complex interplay between inflammatory and neurodegenerative processes across the course of multiple sclerosis (MS) may explain this discrepancy. This paper will provide an up-to-date overview of the rationale and results of the published clinical trials that have sought to alter the trajectory of both primary and secondary MS, considering studies involving drugs with a primary immune target and also those aiming for neuroprotection. Future areas of study will be discussed, building on these results combined with the experience of treating RRMS and new concepts emerging from laboratory science and animal models.

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Stamelou, Maria, and Adam L. Boxer. "Disease-Modifying Treatments for Progressive Supranuclear Palsy." Movement Disorders Clinical Practice 2, no. 1 (February 2, 2015): 3–5. http://dx.doi.org/10.1002/mdc3.12142.

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10

Cummings, Jeffrey L. "Defining and labeling disease-modifying treatments for Alzheimer's disease." Alzheimer's & Dementia 5, no. 5 (September 2009): 406–18. http://dx.doi.org/10.1016/j.jalz.2008.12.003.

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11

Ahlskog, J. Eric. "Considerations for trials of disease modifying treatments in Parkinson disease." Neurology 94, no. 11 (February 26, 2020): 467–68. http://dx.doi.org/10.1212/wnl.0000000000009127.

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12

Zajicek, J. "Diagnosis and disease modifying treatments in multiple sclerosis." Postgraduate Medical Journal 81, no. 959 (September 1, 2005): 556–61. http://dx.doi.org/10.1136/pgmj.2004.031294.

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13

Williams, Owain H., Katharine E. Harding, Mark Willis, Trevor Pickersgill, Mark Wardle, and Neil P. Robertson. "DISEASE MODIFYING TREATMENTS IN MS: INDUCTION OR ESCALATION?" Journal of Neurology, Neurosurgery & Psychiatry 86, no. 11 (October 14, 2015): e4.117-e4. http://dx.doi.org/10.1136/jnnp-2015-312379.29.

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BackgroundIt is currently unclear whether aggressive induction or stepwise escalation of DMTs provides optimum long term outcomes for patients with MS.ObjectiveCompare clinical outcomes in clinical practice amongst unmatched patient groups receiving either initial monoclonal induction, injectable DMT only or escalation from injectable DMT.MethodsA subset of a population-based cohort identified 268 patients, with a median follow up post treatment of 5.4 years. Time to disability end points (EDSS) were examined using survival analysis.ResultsMonoclonals (25%) pre and post treatment annual relapse rate reduced from 2.28 (±1.92) to 0.28 (±0.42) 88% reduction; injectables (62%) from 1.08 (±0.97) to 0.4 (±1.03), 63% reduction; escalation (13%) had elevated rates of 1.72 (±2.04) to 0.64 (±0.54), only 63% reduction. Time to EDSS4 was shorter for monoclonal against injectable and escalation strategies: 5.7 vs 12 vs 6.8 years, p=0.0002. Time to EDSS6 was similar for the treatment strategies respectively: 14.6 vs 16.4 vs 13.3 years, p=0.13.ConclusionsPatients requiring escalation had relatively worse outcomes, and could be identified as having higher disease activity on treatment initiation. This data suggest that initial selection of DMT class does not significantly affect long term outcome to EDSS6, or conversely, aggressive induction slows the rate of disability progression to EDSS6.

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14

Carrithers, Michael D. "Update on Disease-Modifying Treatments for Multiple Sclerosis." Clinical Therapeutics 36, no. 12 (December 2014): 1938–45. http://dx.doi.org/10.1016/j.clinthera.2014.08.006.

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15

Rog, David. "Second-line disease modifying treatments for multiple sclerosis." British Journal of Neuroscience Nursing 7, Sup4 (August 2011): S14—S16. http://dx.doi.org/10.12968/bjnn.2011.7.sup4.s14.

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Feustel, Aden C., Amanda MacPherson, Dean A. Fergusson, Karl Kieburtz, and Jonathan Kimmelman. "Risks and benefits of unapproved disease-modifying treatments for neurodegenerative disease." Neurology 94, no. 1 (December 2, 2019): e1-e14. http://dx.doi.org/10.1212/wnl.0000000000008699.

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ObjectiveTo determine whether patients randomized to unapproved, disease-modifying interventions in neurodegenerative disease trials have better outcomes than patients randomized to placebo by performing a systematic review and meta-analysis of risk and benefit experienced by patients in randomized placebo-controlled trials testing investigational treatments for Alzheimer disease, Parkinson disease, Huntington disease, or amyotrophic lateral sclerosis (ALS).MethodsWe searched MEDLINE, Embase, and ClinicalTrials.gov for results of randomized trials testing non–Food and Drug Administration–approved, putatively disease-modifying interventions from January 2005 to May 2018. Trial characteristics were double-extracted. Coprimary endpoints were the treatment advantage over placebo on efficacy (standardized mean difference in outcomes) and safety (risk ratios of serious adverse events and withdrawals due to adverse events), calculated with random effects meta-analyses. The study was registered on PROSPERO (CRD42018103798).ResultsWe included 113 trials (n = 39,875 patients). There was no significant efficacy advantage associated with assignment to putatively disease-modifying interventions compared to placebo for Alzheimer disease (standardized mean difference [SMD] −0.03, 95% confidence interval [CI] −0.07 to 0.01), Parkinson disease (SMD −0.09, 95% CI −0.32 to 0.15), ALS (SMD 0.02, 95% CI −0.25 to 0.30), or Huntington disease (0.02, 95% CI −0.27 to 0.31). Patients with Alzheimer disease assigned to active treatment were at higher risk of experiencing serious adverse events (risk ratio [RR] 1.15, 95% CI 1.04–1.27) and withdrawals due to adverse events (RR 1.44, 95% CI 1.21–1.70).ConclusionsAssignment to active treatment was not beneficial for any of the indications examined and may have been slightly disadvantageous for patients with Alzheimer disease. Our findings suggest that patients with neurodegenerative diseases are not, on the whole, harmed by assignment to placebo when participating in trials.

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Johnson, C. D., and B. L. Davidson. "Huntington's disease: progress toward effective disease-modifying treatments and a cure." Human Molecular Genetics 19, R1 (April 15, 2010): R98—R102. http://dx.doi.org/10.1093/hmg/ddq148.

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18

Feinstein, Anthony. "Multiple sclerosis, disease modifying treatments and depression: a critical methodological review." Multiple Sclerosis Journal 6, no. 5 (October 2000): 343–48. http://dx.doi.org/10.1177/135245850000600509.

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Background: Major depression affects one in two patients with multiple sclerosis (MS) during the course of their lifetime. This adds to the morbidity associated with the disorder and may contribute to an increased mortality rate because of suicide. Over the past few years, with the advent of disease modifying treatments for MS, a new concern with respect to mood has arisen, namely the possibility that some of these drugs may have depression as a clinically significant side effect. Objective: To ascertain whether disease modifying treatments in MS are associated with the development of depression or the worsening of a depressive illness. Methodology: A MEDLINE and PSYCHLIT search focusing on depression and disease modifying treatments going back to 1993 (the publication date of the results of the first randomised, placebo controlled trial). The methodology pertaining to the assessment of depression is critically reviewed. Furthermore, a critical summary is provided of treatment modalities for the depressed MS patient. Results: There are conflicting data that depression may occur with some disease modifying drugs, particularly interferon beta-1b. However, all studies reveal limitations with respect to the assessment of mood. Some reports, despite omitting details of how mentation was assessed, still comment on the presence or absence of depression. Others suffer from one or more of the following shortcomings: a failure to assess premorbid risk factors for mood disorder; a reliance on one question to assess depression; the utilisation of self report mood rating scales of questionable validity; neglecting to distinguish depression as a symptom from depression as a syndrome (i.e. major depression as defined by the DMS-1V). Conclusions: Given the many methodological pitfalls inherent in all studies to date, it is premature to conclude that disease modifying drugs are associated with depression. Evidence suggests that treatment of depression, irrespective of a putative association with a disease modifying agent, is frequently effective. This applies to pharmacotherapy or psychotherapy, although the former may be preferred should depression arise during a course of treatment with a disease modifying agent.

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19

Galetta, Steven L., and Clyde Markowitz. "US FDA-Approved Disease-Modifying Treatments for Multiple Sclerosis." CNS Drugs 19, no. 3 (2005): 239–52. http://dx.doi.org/10.2165/00023210-200519030-00005.

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20

Cross, A. H., and R. T. Naismith. "Established and novel disease-modifying treatments in multiple sclerosis." Journal of Internal Medicine 275, no. 4 (March 11, 2014): 350–63. http://dx.doi.org/10.1111/joim.12203.

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21

FURST, D. E., F. C. BREEDVELD, G.-R. BURMESTER, L. CROFFORD, P. EMERY, M. FELDMAN, J. R. KALDEN, et al. "Access to disease modifying treatments for rheumatoid arthritis patients." Annals of the Rheumatic Diseases 58, Supplement 1 (November 1, 1999): i129—i130. http://dx.doi.org/10.1136/ard.58.2008.i129.

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22

Oh, Jiwon, and Paul W. O’Connor. "Established disease-modifying treatments in relapsing-remitting multiple sclerosis." Current Opinion in Neurology 28, no. 3 (June 2015): 220–29. http://dx.doi.org/10.1097/wco.0000000000000202.

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23

Giovannoni, Gavin. "Disease-modifying treatments for early and advanced multiple sclerosis." Current Opinion in Neurology 31, no. 3 (June 2018): 233–43. http://dx.doi.org/10.1097/wco.0000000000000561.

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24

WEINBLATT, MICHAEL E., and AGNES L. MAIER. "Disease-Modifying Agents and Experimental Treatments of Rheumatoid Arthritis." Clinical Orthopaedics and Related Research &NA;, no. 265 (April 1991): 103???115. http://dx.doi.org/10.1097/00003086-199104000-00012.

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25

Williams, Owain H., Katharine E. Harding, Mark Willis, Trevor Pickersgill, Mark Wardle, and Neil P. Robertson. "DISEASE MODIFYING TREATMENT UTILISATION IN MULTIPLE SCLEROSIS." Journal of Neurology, Neurosurgery & Psychiatry 86, no. 11 (October 14, 2015): e4.30-e4. http://dx.doi.org/10.1136/jnnp-2015-312379.125.

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BackgroundThe number of disease modifying treatments (DMT) for multiple sclerosis continues to expand, although there is limited data concerning their long term use and utilisation in clinical practice.ObjectiveDescriptive analysis of historic and current DMT utilisation in relation to treatment pathways, course length and discontinuation reasons in real practice.MethodsA subset of a population-based cohort of MS identified 270 patients with prospective data on DMT utilisation, reasons for discontinuation were classified. Descriptive and survival analysis were conducted.Results498 drug initiation events were identified in 270 patients. 2nd line treatment was initiated in 39%, 3rd line=9%, 4th line=3%, 5th line=0.4%, 6th line=0.4%. Commonest DMT initiated was Interferon (67%) followed by Alemtuzumab, with proportional increase in prescription with each line of treatment escalation (1st=19%, 2nd=26%, 3rd=36%). Persistence on first DMT was a median of 1.7 (1.4–2.3) years for Interferon and 2.7 (0.8–5.1) years for Copaxone, excluding fixed course DMTs. Discontinuation occurred on 307 occasions, with the commonest reason being intolerance of side effects in 57%.ConclusionThe greatest limitation to drug efficacy will be its course length and its appropriate utilisation, thus a greater understanding of drug indication and discontinuation will be of benefit in clinical practice.

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Ruthirakuhan, Myuri, Nathan Herrmann, Ivonne Suridjan, Eleenor H. Abraham, Ilan Farber, and Krista L. Lanctôt. "Beyond immunotherapy: new approaches for disease modifying treatments for early Alzheimer’s disease." Expert Opinion on Pharmacotherapy 17, no. 18 (November 22, 2016): 2417–29. http://dx.doi.org/10.1080/14656566.2016.1258060.

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27

Sampaio, Cristina. "Evaluating disease-modifying effects of Alzheimer’s disease treatments: The European regulatory perspective." Alzheimer's & Dementia 1, no. 1 (July 2005): S105—S106. http://dx.doi.org/10.1016/j.jalz.2005.06.366.

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28

Mészáros, Lisa, Alana Hoffmann, Jeanette Wihan, and Jürgen Winkler. "Current Symptomatic and Disease-Modifying Treatments in Multiple System Atrophy." International Journal of Molecular Sciences 21, no. 8 (April 16, 2020): 2775. http://dx.doi.org/10.3390/ijms21082775.

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Multiple system atrophy (MSA) is a rare, severe, and rapidly progressive neurodegenerative disorder categorized as an atypical parkinsonian syndrome. With a mean life expectancy of 6–9 years after diagnosis, MSA is clinically characterized by parkinsonism, cerebellar ataxia, autonomic failure, and poor l-Dopa responsiveness. Aside from limited symptomatic treatment, there is currently no disease-modifying therapy available. Consequently, distinct pharmacological targets have been explored and investigated in clinical studies based on MSA-related symptoms and pathomechanisms. Parkinsonism, cerebellar ataxia, and autonomic failure are the most important symptoms targeted by symptomatic treatments in current clinical trials. The most prominent pathological hallmark is oligodendroglial cytoplasmic inclusions containing alpha-synuclein, thus classifying MSA as synucleinopathy. Additionally, myelin and neuronal loss accompanied by micro- and astrogliosis are further distinctive features of MSA-related neuropathology present in numerous brain regions. Besides summarizing current symptomatic treatment strategies in MSA, this review critically reflects upon potential cellular targets and disease-modifying approaches for MSA such as (I) targeting α-syn pathology, (II) intervening neuroinflammation, and (III) neuronal loss. Although these single compound trials are aiming to interfere with distinct pathogenetic steps in MSA, a combined approach may be necessary to slow down the rapid progression of the oligodendroglial associated synucleinopathy.

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Busse, William W., Erik Melén, and Andrew N. Menzies-Gow. "Holy Grail: the journey towards disease modification in asthma." European Respiratory Review 31, no. 163 (February 22, 2022): 210183. http://dx.doi.org/10.1183/16000617.0183-2021.

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At present, there is no cure for asthma, and treatment typically involves therapies that prevent or reduce asthma symptoms, without modifying the underlying disease. A “disease-modifying” treatment can be classed as able to address the pathogenesis of a disease, preventing progression or leading to a long-term reduction in symptoms. Such therapies have been investigated and approved in other indications, e.g. rheumatoid arthritis and immunoglobulin E-mediated allergic disease. Asthma's heterogeneous nature has made the discovery of similar therapies in asthma more difficult, although novel therapies (e.g. biologics) may have the potential to exhibit disease-modifying properties. To investigate the disease-modifying potential of a treatment, study design considerations can be made, including: appropriate end-point selection, length of trial, age of study population (key differences between adults/children in physiology, pathology and drug metabolism) and comorbidities in the patient population. Potential future focus areas for disease-modifying treatments in asthma include early assessments (e.g. to detect patterns of remodelling) and interventions for patients genetically susceptible to asthma, interventions to prevent virally induced asthma and therapies to promote a healthy microbiome. This review explores the pathophysiology of asthma, the disease-modifying potential of current asthma therapies and the direction future research may take to achieve full disease remission or prevention.

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Judge-Clayden, Florence, Priyanka Iyer, Anna Williams, Katy Murray, and Ruth Dobson. "Multiple sclerosis, disease modifying therapies and pregnancy." British Journal of Neuroscience Nursing 18, Sup3 (July 1, 2022): S22—S26. http://dx.doi.org/10.12968/bjnn.2022.18.sup3.s22.

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Multiple sclerosis (MS) affects women more commonly than men and is often diagnosed between 25 and 37 years of age. Therefore, at the time of diagnosis, many people have not finished trying for a family, and the person with MS often faces questions regarding their disease and the use of treatments when pregnant and breastfeeding. This review provides practical advice and guidance for MS and neurology nurses to help them support people with MS and their families throughout their family planning and pregnancy journeys.

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Guger, Michael, Christian Enzinger, Fritz Leutmezer, Jörg Kraus, Stefan Kalcher, Erich Kvas, and Thomas Berger. "Real‐life use of oral disease‐modifying treatments in Austria." Acta Neurologica Scandinavica 140, no. 1 (April 22, 2019): 32–39. http://dx.doi.org/10.1111/ane.13097.

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Landmeyer, Nils C., Paul-Christian Bürkner, Heinz Wiendl, Tobias Ruck, Hans-Peter Hartung, Heinz Holling, Sven G. Meuth, and Andreas Johnen. "Disease-modifying treatments and cognition in relapsing-remitting multiple sclerosis." Neurology 94, no. 22 (May 19, 2020): e2373-e2383. http://dx.doi.org/10.1212/wnl.0000000000009522.

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ObjectiveDisease-modifying treatments (DMTs) are the gold standard for slowing disability progression in multiple sclerosis (MS), but their effects on cognitive impairment, a key symptom of the disease, are mostly unknown. We conducted a systematic review and meta-analysis to evaluate the differential effects of DMTs on cognitive test performance in relapsing-remitting MS (RRMS).MethodsPubMed, Scopus, and Cochrane Library were searched for studies reporting longitudinal cognitive performance data related to all major DMTs. The standardized mean difference (Hedges g) between baseline and follow-up cognitive assessment was used as the main effect size measure.ResultsForty-four studies, including 55 distinct MS patient samples, were found eligible for the systematic review. Twenty-five studies were related to platform therapies (mainly β-interferon [n = 17] and glatiramer acetate [n = 4]), whereas 22 studies were related to escalation therapies (mainly natalizumab [n = 14] and fingolimod [n = 6]). Reported data were mostly confined to the cognitive domain processing speed. A meta-analysis including 41 studies and 7,131 patients revealed a small to moderate positive effect on cognitive test performance of DMTs in general (g = 0.27, 95% confidence interval [CI] = [0.21–0.33]), but no statistically significant differences between platform (g = 0.27, 95% CI = [0.18–0.35]) and escalation therapies (g = 0.28, 95% CI = [0.19–0.37]) or between any single DMT and β-interferon.ConclusionsDMTs are effective in improving cognitive test performance in RRMS, but a treatment escalation mainly to amend cognition is not supported by the current evidence. Given the multitude of DMTs and their widespread use, the available data regarding differential treatment effects on cognitive impairment are remarkably scant. Clinical drug trials that use more extensive cognitive outcome measures are urgently needed.

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33

Correale, Jorge. "New fungal infections associated with disease-modifying treatments in MS." Multiple Sclerosis Journal 24, no. 7 (April 13, 2018): 1004–6. http://dx.doi.org/10.1177/1352458518770090.

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Ibarra, O., O. Mora, E. Ardanza, A. Lopez de Torre, I. Palacios, and M. Bustos. "Adherence to disease-modifying treatments in patients with multiple sclerosis." European Journal of Hospital Pharmacy 19, no. 2 (March 12, 2012): 240.1–240. http://dx.doi.org/10.1136/ejhpharm-2012-000074.407.

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Dalla Costa, Gloria, Annamaria Finardi, Livia Garzetti, Tiziana Carandini, Giancarlo Comi, Vittorio Martinelli, and Roberto Furlan. "Disease-modifying treatments modulate myeloid cells in multiple sclerosis patients." Neurological Sciences 39, no. 2 (November 28, 2017): 373–76. http://dx.doi.org/10.1007/s10072-017-3176-2.

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Krajnc, Nik, Thomas Berger, and Gabriel Bsteh. "Measuring Treatment Response in Progressive Multiple Sclerosis—Considerations for Adapting to an Era of Multiple Treatment Options." Biomolecules 11, no. 9 (September 10, 2021): 1342. http://dx.doi.org/10.3390/biom11091342.

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Disability in multiple sclerosis accrues predominantly in the progressive forms of the disease. While disease-modifying treatment of relapsing MS has drastically evolved over the last quarter-century, the development of efficient drugs for preventing or at least delaying disability in progressive MS has proven more challenging. In that way, many drugs (especially disease-modifying treatments) have been researched in the aspect of delaying disability progression in patients with a progressive course of the disease. While there are some disease-modifying treatments approved for progressive multiple sclerosis, their effect is moderate and limited mostly to patients with clinical and/or radiological signs of disease activity. Several phase III trials have used different primary outcomes with different time frames to define disease progression and to evaluate the efficacy of a disease-modifying treatment. The lack of sufficiently sensitive outcome measures could be a possible explanation for the negative clinical trials in progressive multiple sclerosis. On the other hand, even with a potential outcome measure that would be sensitive enough to determine disease progression and, thus, the efficacy or failure of a disease-modifying treatment, the question of clinical relevance remains unanswered. In this systematic review, we analyzed outcome measures and definitions of disease progression in phase III clinical trials in primary and secondary progressive multiple sclerosis. We discuss advantages and disadvantages of clinical and paraclinical outcome measures aiming for practical ways of combining them to detect disability progression more sensitively both in future clinical trials and current clinical routine.

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Paraskevas, George P., and Elisabeth Kapaki. "Cerebrospinal Fluid Biomarkers for Alzheimer’s Disease in the Era of Disease-Modifying Treatments." Brain Sciences 11, no. 10 (September 23, 2021): 1258. http://dx.doi.org/10.3390/brainsci11101258.

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Correct in vivo diagnosis of Alzheimer’s disease (AD) helps to avoid administration of disease-modifying treatments in non-AD patients, and allows the possible use of such treatments in clinically atypical AD patients. Cerebrospinal fluid (CSF) biomarkers offer a tool for AD diagnosis. A reduction in CSF β-amyloid (marker of amyloid plaque burden), although compatible with Alzheimer’s pathological change, may also be observed in other dementing disorders, including vascular cognitive disorders due to subcortical small-vessel disease, dementia with Lewy bodies and normal-pressure hydrocephalus. Thus, for the diagnosis of AD, an abnormal result of CSF β-amyloid may not be sufficient, and an increase in phospho-tau (marker of tangle pathology) is also required in order to confirm AD diagnosis in patients with a typical amnestic presentation and reveal underlying AD in patients with atypical or mixed and diagnostically confusing clinical presentations.

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Lindsley, Craig W. "Alzheimer’s Disease: Development of Disease-Modifying Treatments Is the Challenge for Our Generation." ACS Chemical Neuroscience 3, no. 11 (November 21, 2012): 804–5. http://dx.doi.org/10.1021/cn300190f.

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Salloway, Stephen. "Taking the Next Steps in the Treatment of Alzheimer's Disease: Disease-Modifying Agents." CNS Spectrums 13, S3 (March 2008): 11–14. http://dx.doi.org/10.1017/s109285290001720x.

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Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder in the United States and the number of AD patients is increasing at an alarming rate. There is no cure for AD and the currently available treatments are symptomatic, providing only limited effects on disease pathophysiology and progression. An overwhelming need exists for therapies that can slow or halt this debilitating disease process. Disease modification in AD has been defined from patient-focused, regulatory, and neurobiological perspectives. The latter two of these perspectives rely largely on an interruption of the disease process and a clear demonstration of this interruption. As defined by Cummings, a disease-modifying treatment is a “pharmacologic treatment that retards the underlying process of AD by intervening in the neurobiological processes that constitute the pathology and pathophysiology of the disease and lead to cell death or dysfunction.” By this definition, the burden of confirmatory study is placed on any new treatment for which the claim of “disease modification” is to be made (Slide 1).

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Videnovic, Aleksandar, Yo-El S. Ju, Isabelle Arnulf, Valérie Cochen-De Cock, Birgit Högl, Dieter Kunz, Federica Provini, et al. "Clinical trials in REM sleep behavioural disorder: challenges and opportunities." Journal of Neurology, Neurosurgery & Psychiatry 91, no. 7 (May 13, 2020): 740–49. http://dx.doi.org/10.1136/jnnp-2020-322875.

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The rapid eye movement sleep behavioural disorder (RBD) population is an ideal study population for testing disease-modifying treatments for synucleinopathies, since RBD represents an early prodromal stage of synucleinopathy when neuropathology may be more responsive to treatment. While clonazepam and melatonin are most commonly used as symptomatic treatments for RBD, clinical trials of symptomatic treatments are also needed to identify evidence-based treatments. A comprehensive framework for both disease-modifying and symptomatic treatment trials in RBD is described, including potential treatments in the pipeline, cost-effective participant recruitment and selection, study design, outcomes and dissemination of results. For disease-modifying treatment clinical trials, the recommended primary outcome is phenoconversion to an overt synucleinopathy, and stratification features should be used to select a study population at high risk of phenoconversion, to enable more rapid clinical trials. For symptomatic treatment clinical trials, objective polysomnogram-based measurement of RBD-related movements and vocalisations should be the primary outcome measure, rather than subjective scales or diaries. Mobile technology to enable objective measurement of RBD episodes in the ambulatory setting, and advances in imaging, biofluid, tissue, and neurophysiological biomarkers of synucleinopathies, will enable more efficient clinical trials but are still in development. Increasing awareness of RBD among the general public and medical community coupled with timely diagnosis of these diseases will facilitate progress in the development of therapeutics for RBD and associated neurodegenerative disorders.

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Marras, Connie, Laura C. Maclagan, Yi Cheng, Naomi Visanji, Mina Tadrous, and Susan E. Bronskill. "WHAT’S OLD IS NEW: USING ARTIFICIAL INTELLIGENCE TO ACCELERATE DISCOVERY OF NEW TREATMENTS." Innovation in Aging 3, Supplement_1 (November 2019): S16—S17. http://dx.doi.org/10.1093/geroni/igz038.060.

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Abstract Given the high cost of drug development and low success rates, repurposing drugs already proven safe provides a promising avenue for identifying effective therapies with additional indications. The IBM Watson artificial intelligence system was used to search 1.3 million Medline abstracts to prioritize medications that may be potentially disease-modifying in Parkinson’s disease. We assessed patterns of use of the top 50 Watson-ranked drugs among 14,866 adults with Parkinson’s disease aged 70 and older who were matched to persons without Parkinson’s disease on age, sex, and comorbidity. Sociodemographic characteristics, chronic conditions, and use of other medications were compared using standardized differences. Patterns of potentially disease-modifying drug use were examined prior to and following ascertainment of Parkinson’s disease. Preliminary findings from multivariable conditional logistic regression models on the association between previous exposure to potentially disease-modifying drugs and Parkinson’s disease diagnosis will be presented.

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Deepak Chandra Joshi, Harshita, Angana Naskar, Kunal Datta, Urmistha Sarkar, Mihir Kedarbhai Otia, and Tania Khatoon. "Rheumatoid Arthrities: Etiology Pathophysiology and Modern Treatments." International Journal for Research in Applied Sciences and Biotechnology 9, no. 3 (May 15, 2022): 32–39. http://dx.doi.org/10.31033/ijrasb.9.3.7.

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Rheumatoid arthritis (RA) is an autoimmune disease that affects the joints. Age, gender, genetics, and environmental exposure are all factors (cigarette smoking, air pollutants, and occupational). If untreated, felty syndrome, rheumatoid vasculitis, and irreversible joint damage might occur, necessitating splenectomy. Because there is no cure for RA, treatment seeks to reduce pain and prevent further damage. To develop effective RA treatments, researchers must first understand how the disease advances in people and how pathogenic pathways influence this progression. Modern pharmacologic therapy have made tremendous progress in obtaining illness remission without joint deformity (including conventional and biological treatments as well as novel potential small-molecule disease-modifying drugs). Despite this, many RA patients do not respond well to conventional treatments, necessitating the development of novel drugs. This comprehensive review of current advancements covers RA causation, disease-modifying drugs, and prospective RA therapeutics. This section summarises the various RA-related therapies available in the past and now.

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Koyama, Shingo, Yoshiki Sekijima, Masatsune Ogura, Mika Hori, Kota Matsuki, Takashi Miida, and Mariko Harada-Shiba. "Cerebrotendinous Xanthomatosis: Molecular Pathogenesis, Clinical Spectrum, Diagnosis, and Disease-Modifying Treatments." Journal of Atherosclerosis and Thrombosis 28, no. 9 (September 1, 2021): 905–25. http://dx.doi.org/10.5551/jat.rv17055.

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Sekijima, Yoshiki. "Transthyretin (ATTR) amyloidosis: clinical spectrum, molecular pathogenesis and disease-modifying treatments." Journal of Neurology, Neurosurgery & Psychiatry 86, no. 9 (January 20, 2015): 1036–43. http://dx.doi.org/10.1136/jnnp-2014-308724.

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Feinstein, A. "Multiple sclerosis, disease modifying treatments and depression: a critical methodological review." Multiple Sclerosis 6, no. 5 (May 1, 2000): 343–48. http://dx.doi.org/10.1191/135245800678828012.

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Torkildsen, Ø., K. ‐M Myhr, and L. Bø. "Disease‐modifying treatments for multiple sclerosis – a review of approved medications." European Journal of Neurology 23, S1 (November 13, 2015): 18–27. http://dx.doi.org/10.1111/ene.12883.

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Laplaud, David. "Can we discontinue disease-modifying treatments in multiple sclerosis patients? Yes." Revue Neurologique 173, no. 1-2 (January 2017): 38–40. http://dx.doi.org/10.1016/j.neurol.2016.10.005.

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Gouider, R. "Can we discontinue disease-modifying treatments in multiple sclerosis patients? Comments." Revue Neurologique 173, no. 1-2 (January 2017): 44–46. http://dx.doi.org/10.1016/j.neurol.2016.10.006.

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Papeix, C. "Can we discontinue disease-modifying treatments in multiple sclerosis patients? No." Revue Neurologique 173, no. 1-2 (January 2017): 41–43. http://dx.doi.org/10.1016/j.neurol.2016.10.007.

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Andersson, Peter-Brian, Emmanuelle Waubant, and Donald E. Goodkin. "How should we proceed with disease-modifying treatments for multiple sclerosis?" Lancet 349, no. 9052 (March 1997): 586–87. http://dx.doi.org/10.1016/s0140-6736(05)61562-0.

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