Journal
BMC NEUROLOGY
Volume 14, Issue -, Pages -Publisher
BIOMED CENTRAL LTD
DOI: 10.1186/s12883-014-0169-0
Keywords
Late onset Alzheimer's disease; Amyloid cascade hypothesis; Anti-amyloid therapy; Amyloid beta; Familial Alzheimer's disease; Solanezumab; Bapineuzumab; Cholesterol metabolism; Dementia; Neurodegeneration
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Background: High-profile Phase 3 clinical trials of bapineuzumab and solanezumab, antibodies targeted at amyloid-beta (A beta) removal, have failed to meet their primary endpoints. Neither drug improves clinical outcomes in patients with late onset AD, joining a long list of unsuccessful attempts to treat AD with anti-amyloid therapies. Discussion: These therapies are based on the assumption that A beta accumulation is the primary pathogenic trigger of AD. Current evidence suggests that A beta may actually accumulate as part of an adaptive response to long-term chronic brain stress stimuli that would make more suitable candidates for therapeutic intervention. Summary: At this juncture it is no longer unreasonable to suggest that further iterations of anti-A beta therapies should be halted. Clinicians and researchers should instead direct their attention toward greater understanding of the biological function of A beta both in healthy and demented brains, as well as the involvement of long-term chronic exposure to stress in the etiology of AD.
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