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safety
332 studies tagged safety, dated 2000 to 2026-09-09. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
Studies
332 studies carry this tag.
Date range
2000 to 2026
Top journals
- Alzheimer's & dementia : the journal of the Alzheimer's Association 26
- Journal of Alzheimer's disease : JAD 21
- The journal of prevention of Alzheimer's disease 20
- Alzheimer's research & therapy 18
- Alzheimer's & dementia (New York, N. Y.) 14
148 journals in all.
Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.
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Anti-amyloid therapies (AATs), such as anti-amyloid monoclonal antibodies, are emerging treatments for people with early Alzheimer's disease (AD).
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Epilepsy is a cause of profound disability in patients with Alzheimer's disease (AD).
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Alzheimer's disease (AD) research has entered a new era with the recent positive phase 3 clinical trials of the anti-Aβ antibodies lecanemab and donanemab.
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Both act by binding with fibrillary conformations of Aβ plaques in the brain.
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Recently, the U.S. Food and Drug Administration (FDA) approved 2 anti-amyloid monoclonal antibodies, aducanumab (June 7, 2021) and lecanemab (July 6, 2023), for the treatment of Alzheimer's disease (AD) patients, and will most likely also approve a 3rd one, donanemab, soon.
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However, while Aβ may contribute to disease, genetic, clinical, imaging and biochemical data suggest a more complex aetiology.
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Our study suggests that SSAE-3 and SSAE-5 are valid ARIA-E rating scales for use in routine clinical practice by experienced radiologists in specialized settings.
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Alzheimer's disease (AD) has witnessed a gradual rise in its prevalence in recent decades, particularly impacting a substantial segment of individuals aged 85 and above.
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Over the past 30 years, the majority of (pre)clinical efforts to find an effective therapy for Alzheimer's disease (AD) focused on clearing the β-amyloid peptide (Aβ) from the brain since, according to the amyloid cascade hypothesis, the peptide was (and it is still considered by many) the pathogenic determinant of this neurodegenerative disorder.
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Recent Aβ-immunotherapy trials have yielded the first clear evidence that removing aggregated Aβ from the brains of symptomatic patients can slow the progression of Alzheimer's disease.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by cognitive decline and neuronal abnormalities.
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Cellular senescence contributes to Alzheimer's disease (AD) pathogenesis.
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On July 6, 2023, the U.S. Food and Drug Administration (FDA) approved lecanemab (Leqembi) for the treatment of Alzheimer's dementia (AD) patients.
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With recent data demonstrating that lecanemab treatment can slow cognitive and functional decline in early symptomatic Alzheimer disease (AD), it is widely anticipated that this drug and potentially other monoclonal antibody infusions targeting β-amyloid protein will imminently be realistic options for some patients with AD.
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The amyloid cascade hypothesis is a useful framework for therapeutic development in Alzheimer's disease (AD).
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Solanezumab, which targets monomeric amyloid in persons with elevated brain amyloid levels, did not slow cognitive decline as compared with placebo over a period of 240 weeks in persons with preclinical Alzheimer's disease.
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The risk-benefit profile of anti-Aβ monoclonal antibodies (mAbs) in Alzheimer's disease (AD) remains unclear, especially concerning their safety and overall effects on AD progression and cognitive function.
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The US Food and Drug Administration (FDA)'s recent accelerated approval of two anti-amyloid antibodies for treatment of Alzheimer's disease (AD), aducanumab and lecanemab, has caused substantial debate.
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Alzheimer's disease (AD) is a major global public health challenge.
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This study provides the first active comparator data on amyloid plaque clearance in patients with early symptomatic AD.
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The plasma p-tau217 and plasma GFAP models adequately predicted the change over time, with donanemab resulting in decreased plasma p-tau217 and plasma GFAP concentrations.
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Currently, three antibeta amyloid (Aβ) mAbs are approved or under examination in USA and in Europe for the treatment of patients with early Alzheimer's disease.
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In the elderly, a debilitating condition known as dementia, which is a major health concern, is caused by Alzheimer's disease (AD).
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The amyloid cascade model of the pathogenesis of Alzheimer disease (AD) is well supported in observational studies.
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Lecanemab, an anti-amyloid antibody with effects on biomarker and clinical endpoints in early Alzheimer's Disease (AD), was granted accelerated approval by the FDA in 2023 and regulatory review in Europe is ongoing.
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Our analysis found that lecanemab showed significant positive statistical efficacy with respect to cognition, function, and behavior in patients with early AD though the actual clinical significance is yet to be established.
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45/100
Hardy and Mummery discuss the recent positive findings in the clinical trial of lecanemab in early Alzheimer’s disease, and the implications for the amyloid hypothesis.
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Two anti-amyloid monoclonal antibodies (MABs)-lecanemab (Leqembi ® ) and aducanumab (Aduhelm ® )-have been approved in the USA for the treatment of Alzheimer's disease (AD).
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Caregivers and neurologists considered incremental clinical benefit over SOC and safety to be highly desirable qualities for a new drug that could clear amyloid plaques and delay clinical progression and indicated a willingness to accept incremental ARIA-E to achieve additional clinical benefits.
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Pooled MMRM analyses showed a statistically significant effect of solanezumab across cognitive and functional outcome measures.
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43/100
Three deaths have been reported related to treatment with lecanemab.6 Patients receiving DMT require frequent monitoring with MRI brain scans (four or more per year), as there is a high rate of clinically significant amyloid-related imaging abnormalities (ARIA), both brain oedema (ARIA-E) and macro- and microhaemorrhages (ARIA-H).
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Donanemab is an amyloid-targeting therapy that resulted in robust amyloid plaque reduction and slowed Alzheimer's disease (AD) progression compared with placebo in the phase II TRAILBLAZER-ALZ study (NCT03367403).
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After years of failed attempts to develop a disease-modifying therapy for Alzheimer's disease, consistent evidence in support of clinical efficacy was finally presented for a monoclonal antibody targeting the amyloid-β protofibrils.
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40/100
Lecanemab (lecanemab-irmb; LEQEMBI™) is a humanized immunoglobulin gamma 1 (IgG1) against aggregated soluble and insoluble forms of amyloid-β peptide.
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Aducanumab is a novel disease-modifying anti-amyloid-beta (Aβ) human monoclonal antibody specifically targeted to the pathophysiology of Alzheimer's disease (AD).
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Antibody-mediated removal of aggregated β-amyloid (Aβ) is the current, most clinically advanced potential disease-modifying treatment approach for Alzheimer's disease.
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Nonclinical data indicate that ACU193 can reduce the toxic effects of amyloid β oligomers.
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47/100
Lecanemab can be administered without titration with modest incidence of ARIA.
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There are few treatments that slow neurodegeneration in Alzheimer's disease (AD), and while therapeutic antibodies are being investigated in clinical trials for AD treatment, their access to the central nervous system is restricted by the blood-brain barrier.
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Aducanumab is the first FDA-approved amyloid-lowering immunotherapy for Alzheimer's disease.
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Post-hoc analyses showed that outcomes in the ENGAGE high-dose group were affected by an imbalance in a small number of patients with extremely rapid progression and by lower exposure to the target dose of 10 mg/kg.
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A total of 1795 participants were enrolled (lecanemab:898; placebo:897).
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Host responses to anti-amyloid-β (Aβ) antibody therapy are evident in neuroimaging changes and clinical symptoms in a subset of clinical trial subjects receiving such therapy.
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The FDA approved lecanemab for Alzheimer's disease in January 2023 which acts as a novel disease-modifying anti-amyloid-beta (Aβ) human monoclonal antibody and is administered intravenously.
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After the CLARITY-AD clinical trial results of lecanemab were interpreted as positive, and supporting the amyloid hypothesis, the drug received accelerated Food and Drug Administration approval.
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Clinicians specialized in the diagnosis and management of persons living with early-stage Alzheimer's disease need to enable access, for those meeting criteria, to the new class of disease modifying drugs (DMDs).
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Amyloid-β (Aβ) plaques and aggregated tau are two core mechanisms that contribute to the clinical deterioration of Alzheimer’s disease (AD).
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Lecanemab treatment resulted in significant reduction in amyloid plaques and a slowing of clinical decline.
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The results from the gantenerumab phase 3 programs are expected by the end of 2022 and will add critical information to the collective knowledge on the search for effective AD treatments.
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Immunotherapy against amyloid-beta (Aβ) is a promising option for the treatment of Alzheimer's disease (AD).
From across this tag
8 of the 332 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 8. The same 8 appear here every time.
- Bapineuzumab
- Aducanumab, a Novel Anti-Amyloid Monoclonal Antibody, for the Treatment of Alzheimer's Disease: A Comprehensive Review
- Advances of therapeutic strategies for Alzheimer's disease
- Amyloid-related Imaging Abnormalities (ARIA) in the Context of Alzheimer's Disease and Amyloid-targeting Therapies: An Introduction for Advanced Practice Providers
- Aducanumab 36-month data from PRIME: a randomized, double-blind, placebo-controlled Phase 1b study in patients with prodromal or mild Alzheimer’s disease (S2.004)
- Towards pharmacological prevention of Alzheimer disease
- Open questions for Alzheimer's disease immunotherapy
- Disease-modifying therapy for proteinopathies: Can the exception become the rule?