References
- Egan MF , KostJ, VossTet al. Randomized trial of verubecestat for prodromal Alzheimer’s disease. N. Engl. J. Med., 380(15), 1408–1420 (2019).
- Henley D , RaghavanN, SperlingR, AisenP, RamanR, RomanoG. Preliminary results of a trial of atabecestat in preclinical Alzheimer’s disease. N. Engl. J. Med., 380(15), 1483–1485 (2019).
- Forman M , PalczaJ, TsengJet al. Safety, tolerability, and pharmacokinetics of the β-site amyloid precursor protein-cleaving enzyme 1 inhibitor verubecestat (MK-8931) in healthy elderly male and female subjects. Clin. Transl. Sci.doi: https://doi.org/10.1111/cts.12645 (2019) ( Epub ahead of print).
- Cole SL , VassarR. The Alzheimer’s disease-secretase enzyme, BACE1. Mol. Neurodegener., 2(1), 22 (2007).
- Keskin AD , KekušM, AdelsbergerHet al. BACE inhibition-dependent repair of Alzheimer’s pathophysiology. Proc. Natl Acad. Sci. USA, 114(32), 8631–8636 (2017).
- Laird FM , CaiH, SavonenkoAVet al. BACE1, a major determinant of selective vulnerability of the brain to amyloid-β amyloidogenesis, is essential for cognitive, emotional, and synaptic functions. J Neuroscience, 25(50), 11693–11709 (2005).
- Vassar R . Editorial: implications for BACE1 inhibitor clinical trials: adult conditional BACE1 knockout mice exhibit axonal organization defects in the hippocampus. J. Prev. Alzheimers Dis., 6(2), 78–84 (2019).
- Plucińska K , CrouchB, KossDet al. Knock-in of human BACE1 cleaves murine APP and reiterates Alzheimer-like phenotypes. J. Neurosci., 34(32), 10710–10728 (2014).
- Krell-Roesch J , LoweVJ, NeureiterJet al. Depressive and anxiety symptoms and cortical amyloid deposition among cognitively normal elderly persons: the Mayo Clinic Study of Aging. Int. Psychogeriatr., 30(2), 245–251 (2018).
- Krell-Roesch J , VassilakiM, MielkeMMet al. Cortical β-amyloid burden, neuropsychiatric symptoms, and cognitive status: the Mayo Clinic Study of Aging. Transl. Psychiatry, 9(1), 123 (2019).
- Palmqvist S , SchöllM, StrandbergOet al. Earliest accumulation of β-amyloid occurs within the default-mode network and concurrently affects brain connectivity. Nat. Commun., 8(1), 1214 (2017).
- Baker JT , DillonDG, PatrickLMet al. Functional connectomics of affective and psychotic pathology. Proc. Natl Acad. Sci. USA, 116(18), 9050–9059 (2019).
- Busche MA , GrienbergerC, KeskinADet al. Decreased amyloid-β and increased neuronal hyperactivity by immunotherapy in Alzheimer’s models. Nat. Neurosci., 18(12), 1725–1727 (2015).
- Panza F , LozuponeM, LogroscinoG, ImbimboBP. A critical appraisal of amyloid-β-targeting therapies for Alzheimer disease. Nat. Rev. Neurol., 15, 73–88 (2019).
- Pomara N , BrunoD. Basal forebrain resting functional activity associated with brain amyloid-β burden in ε4 carriers and older women: possible implications for baseline cognition and response to amyloid-β-based preventive trials. Radiology, 290(3), 850–851 (2019).