Home > Publications Database > Krankheitsmodifizierende Therapie mit Lecanemab bei früher Alzheimer-Demenz | Disease-modifying therapy with lecanemab for early Alzheimer's dementia > print

001     281871
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024 7 _ |a 0720-4299
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024 7 _ |a 0015-8194
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024 7 _ |a 1439-3522
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037 _ _ |a DZNE-2025-01242
041 _ _ |a German
082 _ _ |a 150
100 1 _ |a Hansen, Niels
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245 _ _ |a Krankheitsmodifizierende Therapie mit Lecanemab bei früher Alzheimer-Demenz | Disease-modifying therapy with lecanemab for early Alzheimer's dementia
260 _ _ |a Stuttgart [u.a.]
|c 2025
|b Thieme
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520 _ _ |a Alzheimer's disease (AD) is a severe and progressive neurodegenerative disease of the brain that has so far been treated with symptomatic drug and non-drug therapies as standard treatment. Following the approval of the monoclonal anti-amyloid antibody by the FDA, AD therapy has changed, as this therapy has made it possible to attenuate the biological disease process of AD. Lecanemab has been recommended by the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency (EMA) for approval in patients with early AD under two conditions. Firstly, homozygous ApoE4 carriers and secondly, patients receiving oral anticoagulants should not receive lecanemab. The following narrative review explains the mechanism of action, safety and side effects of lecanemab. Furthermore, risk factors for side effects are described. Finally, the first experiences with lecanemab are reported and the efficacy and financial aspects are discussed. Lecanemab leads to a temporary reduction in amyloid-ß deposits and to a benefit that can be reflected in everyday competence, cognition and quality of life and can be described as a breakthrough in AD's therapy due to its demonstrable biological and clinical efficacy.
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650 _ 7 |a Antibodies, Monoclonal, Humanized
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650 _ 7 |a Amyloid beta-Peptides
|2 NLM Chemicals
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Alzheimer Disease: drug therapy
|2 MeSH
650 _ 2 |a Alzheimer Disease: psychology
|2 MeSH
650 _ 2 |a Antibodies, Monoclonal, Humanized: therapeutic use
|2 MeSH
650 _ 2 |a Antibodies, Monoclonal, Humanized: adverse effects
|2 MeSH
650 _ 2 |a Amyloid beta-Peptides: metabolism
|2 MeSH
700 1 _ |a Wiltfang, Jens
|0 P:(DE-2719)2811317
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773 _ _ |a 10.1055/a-2681-4558
|g Vol. 93, no. 11, p. 453 - 460
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|t Fortschritte der Neurologie, Psychiatrie
|v 93
|y 2025
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856 4 _ |y OpenAccess
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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