But then again, if someone had told you about a study relating stress and anything, you’d have to put your money on stress making it worse.

Green et al. administered the stress hormone dexamethasone to mice, and found that this treatment increases the steady state levels of Aß and tau in both young and old animals.

Various environmental and genetic factors influence the onset and progression of Alzheimer’s disease (AD). Dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis, which controls circulating levels of glucocorticoid hormones, occurs early in AD, resulting in increased cortisol levels. Disturbances of the HPA axis have been associated with memory impairments and may contribute to the cognitive decline that occurs in AD, although it is unknown whether such effects involve modulation of the amyloid beta-peptide (Aß) and tau. Using in vitro and in vivo experiments, we report that stress-level glucocorticoid administration increases Aß formation by increasing steady-state levels of amyloid precursor protein (APP) and ß-APP cleaving enzyme. Additionally, glucocorticoids augment tau accumulation, indicating that this hormone also accelerates the development of neurofibrillary tangles. These findings suggest that high levels of glucocorticoids, found in AD, are not merely a consequence of the disease process but rather play a central role in the development and progression of AD.

Originally I suspected that this might be the result of diminished immune surveillance: Stress hormones are immune suppressive — as Robert Sapolsky is often fond of pointing out, there’s no use worrying about that runny nose when you’re running away from a saber-toothed tiger — and there are sound reasons to believe that immune surveillance could play a role in decreasing Aß levels. The data here, however, quite clearly indicate that dexamethasone is driving up the rates of Aß synthesis, which is sufficient to explain the increase in steady-state Aß levels (though I suppose these data don’t rule out a further negative effect on immune clearance).

In any event: Here Alzheimer’s is revealed as not only a disease of aging (which it certainly is, at least in its more common form; new light on this has been cast by recent results in the worm) but also a disease of stress. We’ve also recently seen a connection drawn between elevated stress hormones and shortened telomeres, in a study that also points to telomere shortening as a marker for the risk of age-related disease.

So get busy living or get busy dying, but don’t get too busy, because that stress will rot your brain.