Abstract
Numerous amyloid-based clinical studies have recently failed. Does this mean that the mechanisms of Alzheimer's disease have to be reinvestigated and that amyloid is not the trigger of the disease? Strong genetic evidence from familial Alzheimer's disease contradicts this fatalistic opinion. Mutations in all genes associated with familial Alzheimer's disease affect amyloid metabolism and aggregation. Moreover, a protective mutation reduces amyloid production by 20-30% throughout the lifetime. Clinical studies rather failed because secretase inhibitors block cleavage of numerous other physiologically important substrates of secretases. Moreover, the disease is initiated decades before symptoms occur. Successful treatment attempts with anti-amyloid medication based on other prototype amyloidoses are described. Finally, new therapeutic target molecules expressed in microglia cells are discussed.
Dokumententyp: | Zeitschriftenartikel |
---|---|
Fakultät: | Medizin
Medizin > Munich Cluster for Systems Neurology (SyNergy) |
Themengebiete: | 600 Technik, Medizin, angewandte Wissenschaften > 610 Medizin und Gesundheit |
URN: | urn:nbn:de:bvb:19-epub-79252-7 |
ISSN: | 0028-2804 |
Sprache: | Englisch |
Dokumenten ID: | 79252 |
Datum der Veröffentlichung auf Open Access LMU: | 15. Dez. 2021, 14:47 |
Letzte Änderungen: | 05. Aug. 2024, 08:04 |
DFG: | Gefördert durch die Deutsche Forschungsgemeinschaft (DFG) - 390857198 |