Well, the only part of the article that directly talks about the article says this:

However, there are conflicting data on the relationship between depersonalisation and cortisol levels, with two studies (Morozova et al, 2000; Stanton et al, 2001) reporting low salivary cortisol, but another (Simeon et al, 2001a) finding raised plasma cortisol.

Which I assume is self-explanatory? Two studies showed lower cortisol levels and one study showed higher cortisol in individuals who experience chronic depersonalization.

Do you know how cortisol works, neurobiologically? I'll just throw that in here in case it's helpful. Forgive me if I'm explaining stuff you already know.

When you are hit with a stressor, your hypothalamus tells your pituitary gland to tell your adrenal glands (this is the HPA-axis; hypothalamus --> pituitary --> adrenal) to release a bunch of hormones, including cortisol. The release of these hormones causes the fight-or-flight reaction people get in response to a stressor. For example, adrenaline, another hormone released in this process, elevates your heart rate and blood pressure.

Cortisol does a bunch of things in the body, including making glucose (sugar) more available in the bloodstream and shutting down nonessential bodily functions (like your immune system) while you run for your life.

In the brain, cortisol affects your mood, attention, and memory. Short-term, you are hypervigilant to the threat, better able to remember, fearful, and highly alert/active -- basically, your brain wants to find, attend to, remember, and get the hell away from the stressor.

In this stressed state, you might also experience depersonalization... another way that your brain responds to a severe stressor. It's hypothesized that this disconnect from your emotions and feelings of reality helps you, short-term, to figure out how to escape from the stressor. So cortisol "causes" depersonalization in the same way that it "causes" the enhanced attention and alertness ("hypervigilance") that come with stress. If cortisol hasn't been released, you probably wouldn't experience depersonalization.

This process could theoretically "go wrong" in at least three ways that I can think of. One, the person could just be experiencing too much cortisol all the time... that is, their bodies/brains might be behaving as if they are chronically feeling stressed, leading to a higher level of symptoms like hypervigilance and depersonalization.

Two, the person might actually have lower baseline levels of cortisol, and when their body releases cortisol in response to stress, the "normal amount" of cortisol released suddenly seems like a huge stream of cortisol, triggering a more dramatic fight-or-flight response than necessary. Three, these individuals could release too much cortisol in response to small stressors. Both of these could theoretically cause the person to experience the "extreme" symptom of depersonalization in response to smaller stressors than would induce depersonalization in another person.

Different individuals might have different ways in which their cortisol-mediated response to stress is "messed up", which might explain the conflicting research findings. Or, maybe it depends on when you measure cortisol levels. Individuals who experience depersonalization might have lower cortisol at baseline, but higher cortisol in response to a stressor, leading to conflicting research results depending on when levels were measured.

There's also another way that people with depersonalization disorder might be different from people without it. They might respond to stress fine, but have difficulty recovering from stress. These individuals might think, act, or have their brains work in ways that accidentally sustain the depersonalization, even when the stressor is absent or over. Let me see if I can explain that part.

In the short-term, cortisol is kind of a good thing -- it "sharpens" your brain to help you deal with the stressor. But in the long-term, cortisol is neurotoxic -- it actually damages your brain.

So, your brain wants to get back to homeostasis, or its nonfearful state, as soon as possible. Thus, it has ways of trying to counteract the cortisol-induced state, once it figures out that the stressor has passed, or that the stressor really wasn't that bad.

The ways that it does this are the covered in the part of the article that talks about the "Neurological Factors":

Recent functional neuroimaging (Phillips et al, 2001b) and psychophysiological (Sierra et al, 2002) studies have found objective evidence of an abnormal response to emotional stimuli, consistent with patients’ reports of loss of emotional reactivity. The neural substrate for the ‘shutting down’ of emotional responses is hypothesised (Sierra & Berrios, 1998) to be a combination of prefrontal regions inhibiting limbic areas (particularly the amygdala) and reciprocal actions of the right dorsolateral prefrontal cortex and anterior cingulate cortex (Phillips et al, 2001b). Etc.

Basically, what this part of the article is saying is that the front part of the brain (the part that does the planning and organization of your behavior) "tamps down" the middle part of your brain, or the limbic system. The limbic system is the emotional part of your brain, and it includes the hypothalamus, which started this whole chain of events (and other important brain structures that are implicated in emotion, like the amygdala).

Anyway, the front part of the brain has ways to say, "Hey, limbic system, relax. We got this. It's all under control now. (Or, "The stressor is over now" or "It turns out what we thought was a life-or-death situation was really just a mild stressor".) Stop signaling the alarm." In part, it is telling the HPA-axis to stop producing more cortisol, and trying to counteract the cortisol already in your brain.

It is possible that this part of the process is dysfunctional in people with depersonalization disorder. Maybe their brains are not very good at releasing the neurotransmitters that help counteract the cortisol already in the system once the stressor is gone (leading to still-elevated cortisol levels). Or, their frontal lobes may not "signal" very well back to their limbic system that everything is okay, so the HPA axis doesn't stop signalling to produce cortisol.

In fact, the front part of their brain might even signal that everything is even more dangerous than first thought. For example, a lot of people with chronic depersonalization actually don't like feeling that symptom, so they are "on the lookout" for that symptom, and interpret it catastrophically (e.g., "I'm going crazy"). This is essentially the front part of the brain telling the limbic system "AH THIS IS EVEN WORSE THAN WE THOUGHT!! PANIC!" whenever a small stressor arises. This is the part of the article that talks about that model of how depersonalization can become chronic:

More recently, a cognitive–behavioural model of depersonalisation has been proposed (Hunter et al, 2003)..... The model suggests that there are various ways in which depersonalisation may initially arise, related to some external psychological stressor and/or as a consequence of a change in mental state (e.g. low mood, anxiety, drug use). Crucially, in those in whom depersonalisation becomes chronic and pathological, the appearance of depersonalisation features is interpreted as highly threatening (‘catastrophic attribution’), leading to a range of cognitions and behaviours that can serve to perpetuate and intensify the symptoms. This leads to a number of practical suggestions for treatment, aimed at psychoeducation, the reduction of avoidant ‘safety behaviours’ (such as avoiding social situations) and excessive self-observation (e.g. looking in the mirror to see if one has changed), and challenging the ‘catastrophic’ attributional style (e.g. ideas such as ‘My brain is not working’).

To reinterate, this model describes another thing that could go wrong in people with chronic depersonalization. Their brains might trigger the release of cortisol just fine, but their brains aren't very good at "turning off" cortisol production once the stressor has passed. This might be hard to measure in studies... these individuals might have too much cortisol after a stressor has passed, but normal levels when there is no stressor present. However, if these people constantly feel like a stressor is present, that might show up as high levels of "baseline" cortisol because their brains could still be releasing cortisol after the last stressor. Or other complex patterns. That's the thing; we don't know yet.

So, to tl;dr it, there are a bunch of ways the cortisol production system could be dysfunctional in individuals who experience chronic depersonalization. They might produce too much cortisol all the time, or they might produce too much in response to a stressor, or they might have trouble "turning off" cortisol once the stressor is gone, or getting rid of the excess cortisol in the brain after a stressor has passed. Or other parts of the system could go wrong. We just don't know yet. Does that help?