Journal
MOLECULAR PSYCHIATRY
Volume 26, Issue 1, Pages 296-308Publisher
SPRINGERNATURE
DOI: 10.1038/s41380-020-0721-9
Keywords
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Funding
- Swedish Research Council [2018-02532]
- European Research Council [681712]
- Swedish State Support for Clinical Research [ALFGBG-720931]
- UK Dementia Research Institute at UCL
- National Institute on Aging [P30AG062715, R01AG037639, RF1AG059312, R01AG062285, RF1AG057784, UF1AG051216]
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Clinical trial results indicate that antibody-based removal of Aβ plaques may slow cognitive decline in symptomatic AD, highlighting the need to identify suitable biomarkers for treatment. Further research into copathologies is necessary to facilitate the development and implementation of novel drug candidates against AD.
Clinical trial results presented in 2019 suggest that antibody-based removal of cerebral amyloid beta (A beta) plaques may possibly clear tau tangles and modestly slow cognitive decline in symptomatic Alzheimer's disease (AD). Although regulatory approval of this approach is still pending, preparing the healthcare system for the advent of disease-modifying therapies against AD is imperative. In particular, it will be necessary to identify the most suitable biomarkers to facilitate appropriate treatment of AD. Here, we give an update on recent developments in fluid and imaging biomarkers for AD-related pathologies and discuss potential approaches that could be adopted to screen for and clarify the underlying pathology in people seeking medical advice because of cognitive symptoms. We succinctly review recent data regarding biomarkers for A beta and tau pathology, neurodegeneration, synaptic dysfunction, and inflammation, highlight the need for further research into common copathologies, and suggest how different biomarkers could be used (most likely in combination) to facilitate the development and clinical implementation of novel drug candidates against AD.
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