Journal Article Review Epublish 14 citations
PubMed: 39595200 DOI: 10.3390/biomedicines12112636
Disease Modifying Monoclonal Antibodies and Symptomatic Pharmacological Treatment for Alzheimer's Disease.
Biomedicines 12(11)
Authors: Xiaoming Qi, Damir Nizamutdinov, Song Stephen Yi, Erxi Wu, Jason H Huang
Affiliations
- Department of Neurology, Baylor Scott & White Health, Temple, TX 78508, USA.
- Department of Neurosurgery, Neuroscience Institute, Baylor Scott & White Health, Temple, TX 78508, USA.
- Department of Neurosurgery, Neuroscience Institute, Baylor Scott & White Health, Temple, TX 78508, USA. Department of Neurosurgery, Baylor College of Medicine, Temple, TX 76508, USA. College of Medicine, Texas A&M University, College Station, TX 77843, USA. College of Irma Lerma Rangel College of Pharmacy, Texas A&M University, College Station, TX 77843, USA. LIVESTRONG Cancer Institutes, Department of Oncology, Dell Medical School, The University of Texas at Austin, Austin, TX 78712, USA.
- Department of Neurosurgery, Baylor College of Medicine, Temple, TX 76508, USA.
- College of Medicine, Texas A&M University, College Station, TX 77843, USA.
Abstract
Alzheimer's Disease (AD) is an irreversible, progressive syndrome characterized by neurocognitive impairment. Two neuropathological features seen in AD are extracellular amyloid plaques consisting of amyloid beta1-40 and 1-42, and intracellular neurofibrillary tangles (NFTs). For decades, neuroscience research has heavily focused on seeking to understand the primary mechanism of AD and searching for pharmacological approaches for the treatment of dementia. Three monoclonal antibodies that act against amyloid beta-aducanumab, lecanemab, and donanemab-have been approved by the Food and Drug Administration (FDA) for the treatment of mild cognitive impairment and mild AD, in addition to medications for cognitive symptom management such as acetylcholinesterase inhibitors and the N-methyl-D-aspartate (NMDA) antagonist. Further trials should focus on the combination of therapies targeting amyloid plaques and tau pathology.
MeSH
Plaque, Amyloid, Antibodies, Alzheimer Disease, Cognitive Dysfunction, Cognition Disorders, Antibodies, Monoclonal, Therapeutics, Amyloid
Cited by
- Lecanemab for mild Alzheimer disease - is there a way forward? Drugs Context, 2025
- Synthesis, Biological Evaluation, and Molecular Docking Studies of Novel Coumarin-Triazole-Isatin Hybrids as Selective Butyrylcholinesterase Inhibitors. Molecules, 2025
- Binding of Pro-Inflammatory Proteins S100A8 or S100A9 to Amyloid-β Peptide Suppresses Its Fibrillation. Biomolecules, 2025
- Dysregulation of Astrocytic ATP/Adenosine Release in the Hippocampus Cause Cognitive and Affective Disorders: Molecular Mechanisms, Diagnosis, and Therapy. MedComm (2020), 2025
- Δ133p53α-mediated inhibition of astrocyte senescence and neurotoxicity as a possible therapeutic approach for neurodegenerative diseases. Neuroscience, 2025