Thanks for posting koo.

I've pulled some excerpts from the discussion section of the research paper. This illustrates the problem precisely. 

Excerpts From Journal Of Alzheimer’s Disease Oct 12 , 2021

J Alzheimers Dis. 2021; 83(4): 1703–1715.

Published online 2021 Oct 12. Prepublished online 2021 Aug 24. doi: 10.3233/JAD-210570

Note - underlining and bolding is mine. 

Apabetalone is a small molecule BETi and in the BETonMACE trial, was associated with an 18% favorable trend towards a lower risk of the composite MACE endpoint (p = 0.11) and a 41% reduction in hospitalization for congestive heart failure (p = 0.03) [17–19].

The treatment-placebo difference on the MoCA for those with baseline scores of 21 or less was 2.1 (1.7 for the placebo group; 3.8 for the treatment group; p = 0.03). This 2.1-point difference is in the upper range of the minimum clinically important difference (MCID) of MoCA scores which varies between 1.22 and 2.15 in a similar (post-stroke) population treated with rehabilitation [21]. This outcome is sufficiently promising to warrant further investigation into the possible beneficial effects of apabetalone on cognition in patients with dementia of AD, vascular, or mixed etiology.

Effects may include reduction of vascular inflammation and calcification, modulation of the complement and coagulation cascades, decrease in lipid levels, and reduced systemic inflammation, as have previously been reported for apabetalone [36, 37].

Apabetalone suppresses BBB endothelial cell secretion of cytokines and chemokines and reduces the abundance of surface adhesion molecules in vitro. It lowers monocyte chemokine receptor expression, and monocyte chemoattraction [47]. As a result, apabetalone prevents the binding of monocytes to BBB endothelial cells stimulated by cytokines [47].

As a result, apabetalone prevents the binding of monocytes to BBB endothelial cells stimulated by cytokines [47].

Apabetalone is proposed to protect the BBB by reducing systemic and local inflammation, resulting in less neuroinflammation and decreased neurodegeneration.

Alkaline phosphatase has previously been shown to decrease in apabetalone-treated patients in studies of CVD or CKD patients [25]. In this cognition sub-study, alkaline phosphatase levels decreased significantly in the apabetalone-treatment subgroup compared to the placebo group across all pre-defined cognitive subgroups

This study has important limitations. Dichotomization of the study population at age 70 years was arbitrary but intended to focus on patients at high risk for cognitive decline. . Effects of apabetalone on cognition in younger patients are unknown.

 My thought - with this success why has zero progress been made in the past 3 years? 

The lack of progress is unexplainable to me.

GLTA

Toinv