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anti-amyloid-therapy
9 studies tagged anti-amyloid-therapy, dated 2005-01-01 to 2026-11-09. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
- Rapid Apolipoprotein E ε4 Proteotyping for Alzheimer's Disease Anti-Amyloid Therapy Eligibility and Risk Assessment 2026-11-09
- Acute Neurologic Decline in the ED: A Case Report on Recognizing ARIA in the Age of Anti-Amyloid Therapy 2026-10-31
- Baseline MRI markers and clinical outcomes during anti-amyloid β therapy: A real-world study in a Japanese dementia center 2026-10-17
Studies
9 studies carry this tag.
Date range
2005 to 2026
Top journals
- Alzheimer's & dementia : the journal of the Alzheimer's Association 1
- Annals of medicine and surgery (2012) 1
- BMC neurology 1
- CNS drugs 1
- International journal of nanomedicine 1
9 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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Proteotyping reliably rules out E4/E4 homozygosity (100% NPV), enabling rapid eligibility screening for anti-amyloid therapies.
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Anti-amyloid beta (Aβ) immunotherapies are an emerging treatment for Alzheimer's disease (AD) with a rare but significant risk of amyloid-related imaging abnormalities (ARIA).
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Baseline medial temporal atrophy was associated with functional decline and microbleeds with ARIA-H. Pretreatment MRI may provide prognostic and safety information during anti-amyloid β therapy.
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Anti-amyloid monoclonal antibodies provide disease-modifying treatment options for selected patients with early symptomatic Alzheimer disease, but introduce new challenges for acute stroke care.
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The global burden of Alzheimer's disease (AD) is accelerating, with U.S. prevalence projected to reach nearly 13 million by 2060.
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Anti-amyloid drugs for early Alzheimer's disease, including lecanemab, are associated with adverse events (AEs), such as amyloid-related imaging abnormalities (ARIA)-edema/effusion (E), ARIA-hemorrhage, and infusion-related reactions, which can indicate allocated arms in clinical trials.
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Recent successive approval of anti-amyloid-β (Aβ) monoclonal antibodies as disease-modifying therapies against Alzheimer's disease (AD) has raised great confidence in the development of anti-AD therapies; however, the current therapies still face the dilemma of significant adverse reactions and limited effects.
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These therapies are based on the assumption that Aβ accumulation is the primary pathogenic trigger of AD.
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The leading hypothesis of the pathophysiology of Alzheimer's disease holds that the pivotal event is cleavage of the amyloid precursor protein to release intact the 42-amino-acid amyloid-beta peptide (Abeta); this hypothesis best explains the known genetic causes of Alzheimer's disease.