Dr. Cheryl Wellington's group from Univ. of British Columbia were the authors of this new review and they have published an excellent previous review on this similar topic back in 2014. 

High-Density Lipoproteins and Cerebrovascular Integrity in Alzheimer’s Disease

https://www.ncbi.nlm.nih.gov/pubmed/24508505

https://www.cell.com/cell-metabolism/fulltext/S1550-4131(14)00009-6

This paper was also published post-ASSURE and post-ASSURE post-hoc and was a lot kinder to RVX-208 (other than mistakenly referring to it as RVS-208):

"RVX208: A Small Molecule ApoA-I Modulator

RVX208 is a first in class small molecule that increases endogenous apoA-I production and is currently in development for acute coronary syndrome, atherosclerosis, and AD (Bailey et al., 2010). RVS208 was recently evaluated in the Phase 2b ASSURE clinical trial, which is a 26-week, double-blind, randomized, parallel group, placebo-controlled trial with 324 subject with low HDL-C levels. The RVX208-treated group demonstrated reduced coronary atheroma volume, increased apoA-I levels, and increased HDL-C levels (Nicholls et al., 2012). Although this study did not meet its primary endpoint, a third party analysis of the ASSURE data showed that patients receiving RVS208 in combination with rosuvastatin had a highly statistically significant plaque reduction of 1.43%, exceeding the prespecified primary endpoint by more than 2-fold (Resverlogix, 2013).

With respect to AD, an exploratory Phase Ia trial that enrolled 24 subjects for a double-blind, placebo-controlled, dose-escalation study for a period of 7 days was reported by Resverlogix to lead to a clear but nonsignificant trend toward a 12%–14% increase in plasma Aβ40 levels at 8 mg/kg dose after 7 days of dosing compared with controls (Resverlogix, 2008). In the ASSERT Phase II randomized, placebo-controlled, dose-ranging study of 299 patients with stable coronary artery disease, 150 mg of RVX208 (twice daily) led to a significant increase in plasma Aβ40 levels from baseline and, in the quartile of patients with the lowest plasma Aβ40 levels at baseline, a 13.4% increase in plasma Aβ40 levels compared with placebo (Resverlogix, 2011). These intriguing observations support the hypothesis that RVX208 can stimulate the release of Aβ40 from the brain, consistent with the effects of genetic upregulation of apoA-I levels in AD mice. Further evaluations of RVS208 in the modulation of AD pathogenesis using double-blind placebo-controlled clinical trials are eagerly awaited."