Dementia with Lewy Bodies Drug Therapies in Clinical Trials: Systematic Review up to 2022

Abdelnour, Carla; González, María; Gibson, Lucy; Poston, Kathleen L.; Ballard, Clive; Cummings, Jeffrey L.; Aarsland, Dag

doi:10.1007/s40120-023-00467-8

Cited by 6 publications

(2 citation statements)

References 39 publications

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“…Dag Aarsland, King’s College London, UK, discussed various facets of dementia treatment, including current drug therapies, the drug pipeline for AD, and the significance and considerations of new anti-amyloid monoclonal antibodies such as lecanemab and donanemab. He also explored treatment approaches for Lewy body disease, the potential for prevention through lifestyle changes, and the role of the Norwegian Anti-Dementia Drug Trial Platform (NORADD-TP) ( 68 ). He highlighted the development of 3 new anti-amyloid drugs, promising early results with anti-tau and anti-alpha synuclein drugs, and the potential of repurposed drugs and supplements.…”

Section: Diagnosis and Interventionsmentioning

confidence: 99%

Meeting Summary of The NYO3 5th NO-Age/AD Meeting and the 1st Norway–UK Joint Meeting on Aging and Dementia: Recent Progress on the Mechanisms and Interventional Strategies

Wang,

Siow,

Schmauck-Medina

et al. 2024

The Journals of Gerontology, Series A: Biological Sciences and Medical Sciences

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Unhealthy ageing poses a global challenge with profound healthcare and socioeconomic implications. Slowing down the ageing process offers a promising approach to reduce the burden of a number of age-related diseases, such as dementia, promoting healthy longevity in the old population. In response to the challenge of the ageing population and with a view to the future, Norway and the UK are fostering collaborations, supported by a "Money Follows Cooperation agreement" between the two nations. The inaugural Norway-UK joint meeting on ageing and dementia gathered leading experts on ageing and dementia from the two nations to share their latest discoveries in related fields. Since ageing is an international challenge, and to foster collaborations, we also invited leading scholars from 11 additional countries to join this event. This report provides a summary of the conference, highlighting recent progress on molecular ageing mechanisms, genetic risk factors, DNA damage and repair, mitophagy, autophagy, as well as progress on a series of clinical trials (e.g., using NAD+ precursors). The meeting facilitated dialogue among policy makers, administrative leaders, researchers, and clinical experts, aiming to promote international research collaborations and to translate findings into clinical applications and interventions to advance healthy ageing.

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Section: Diagnosis and Interventionsmentioning

confidence: 99%

Meeting Summary of The NYO3 5th NO-Age/AD Meeting and the 1st Norway–UK Joint Meeting on Aging and Dementia: Recent Progress on the Mechanisms and Interventional Strategies

Wang,

Siow,

Schmauck-Medina

et al. 2024

The Journals of Gerontology, Series A: Biological Sciences and Medical Sciences

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“…As a result of misdiagnosis/late diagnosis and the lack of validated, widely available biomarkers outside of the research setting and approved treatments, there is insufficient public awareness, limited patient advocacy, and hence less funding for basic research. So, not surprisingly, very few therapeutic options are available, and there is comparatively little in the Research and Development pipeline 13,14 …”

Section: Introductionmentioning

confidence: 99%

Lewy body dementia: Overcoming barriers and identifying solutions

Agarwal,

Backler,

Bayram

et al. 2024

Alzheimer's & Dementia

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Despite its high prevalence among dementias, Lewy body dementia (LBD) remains poorly understood with a limited, albeit growing, evidence base. The public‐health burden that LBD imposes is worsened by overlapping pathologies, which contribute to misdiagnosis, and lack of treatments. For this report, we gathered and analyzed public‐domain information on advocacy, funding, research outputs, and the therapeutic pipeline to identify gaps in each of these key elements. To further understand the current gaps, we also conducted interviews with leading experts in regulatory/governmental agencies, LBD advocacy, academic research, and biopharmaceutical research, as well as with funding sources. We identified wide gaps across the entire landscape, the most critical being in research. Many of the experts participated in a workshop to discuss the prioritization of research areas with a view to accelerating therapeutic development and improving patient care. This white paper outlines the opportunities for bridging the major LBD gaps and creates the framework for collaboration in that endeavor.Highlights A group representing academia, government, industry, and consulting expertise was convened to discuss current progress in Dementia with Lewy Body care and research. Consideration of expert opinion,natural language processing of the literature as well as publicly available data bases, and Delphi inspired discussion led to a proposed consensus document of priorities for the field.

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Targeting Lewy body dementia with neflamapimod‐rasagiline hybrids

Albertini,

Petralla,

Massenzio

et al. 2024

Archiv der Pharmazie

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Lewy body dementia (LBD) represents the second most common neurodegenerative dementia but is a quite underexplored therapeutic area. Nepflamapimod (1) is a brain‐penetrant selective inhibitor of the alpha isoform of the mitogen‐activated serine/threonine protein kinase (MAPK) p38α, recently repurposed for LBD due to its remarkable antineuroinflammatory properties. Neuroprotective propargylamines are another class of molecules with a therapeutical potential against LBD. Herein, we sought to combine the antineuroinflammatory core of 1 and the neuroprotective propargylamine moiety into a single molecule. Particularly, we inserted a propargylamine moiety in position 4 of the 2,6‐dichlorophenyl ring of 1, generating neflamapimod‐propargylamine hybrids 3 and 4. These hybrids were evaluated using several cell models, aiming to recapitulate the complexity of LBD pathology through different molecular mechanisms. The N‐methyl‐N‐propargyl derivative 4 showed a nanomolar p38α‐MAPK inhibitory activity (IC50 = 98.7 nM), which is only 2.6‐fold lower compared to that of the parent compound 1, while displaying no hepato‐ and neurotoxicity up to 25 μM concentration. It also retained a similar immunomodulatory profile against the N9 microglial cell line. Gratifyingly, at 5 μM concentration, 4 demonstrated a neuroprotective effect against dexamethasone‐induced reactive oxygen species production in neuronal cells that was higher than that of 1.

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Dementia with Lewy Bodies Drug Therapies in Clinical Trials: Systematic Review up to 2022

Cited by 6 publications

References 39 publications

Meeting Summary of The NYO3 5th NO-Age/AD Meeting and the 1st Norway–UK Joint Meeting on Aging and Dementia: Recent Progress on the Mechanisms and Interventional Strategies

Meeting Summary of The NYO3 5th NO-Age/AD Meeting and the 1st Norway–UK Joint Meeting on Aging and Dementia: Recent Progress on the Mechanisms and Interventional Strategies

Lewy body dementia: Overcoming barriers and identifying solutions

Targeting Lewy body dementia with neflamapimod‐rasagiline hybrids

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