Ketosis is simply the process of your body hydrolyzing (chemical breakdown via the interjection of a water molecule to form two end products, or the reaction of a substrate with water) stored triglycerides (fatty acid chains combined with a glycerol, and the body's primary source of stored adipose) to be used as fuel; Ketosis is the recognition by your body of chronic starvation. It therefore causes lipolysis (breakdown of stored triglycerides into respective fatty acids and glycerol molecules) in order to provide fuel in the absence of glucose (your body uses these as fuel via B-Oxidation). AP is beneficial, because it will expedite (speed up) this process due to its direct interconnectivity with many of the above mentioned processes.
a) It increases levels of CPT-1. CPT-1 is the rate-limiting (controls the rate at which a process can occur) enzyme of B-Oxidation (the oxidizing of fatty acids to be used as fuel), and increasing it increases the amount of lipids your mitochondria will use as fuel. This is important, because even during Ketosis where lipolysis (break up of TG into FAs) is occurring, if you do not oxidize (burn) the FAs, they will simply redeposit.
b) On the note of redepositing, AMPk inhibits the accumulation and synthesis of TGs and cholesterol. Why is this beneficial, and tied into the above point? Because if the redepositing of lipids is inhibited, they will be forced to circulate the bloodstream continually; with the increasing of CPT-1, the possibility is increased they will subsequently be oxidized.
Now, as I said, R-ALA is not an anti-lipogenic (compound which inhibits the accumulation, differentiation, or biosynthesis of lipids) and would not assist as greatly as AP would on a "carb-up" during Ketosis. The primary goal of Ketosis is releasing stored triglycerides into the bloodstream to be oxidized: AP accomplishes this. The fundamental step to remaining in Ketosis is low blood sugar levels: AP accomplishes this.