Researchers at the Salk Institute for Biological Studies have found in a study of mice that repeated emotional stress, the kind humans experience in everyday life, may contribute to the accumulation of neurofibrillary tangles in the animal, which is a hallmark of Alzheimers disease.
The researchers say that while aging is still the greatest risk factor for Alzheimers disease, a number of studies have pointed to stress as a contributing factor.
A long-term study of about 800 members of religious orders had found that the people who were most prone to stress were twice as likely to develop Alzheimers disease, but the nature of the link between the two has been elusive, says lead researcher Dr. Paul E. Sawchenko, a professor in the Neuronal Structure and Function Laboratory.
The study, published in the Journal of Neuroscience, suggests that the brain-damaging effects of negative emotions are relayed through the two known corticotropin-releasing factor receptors, namely CRFR1 and CRFR2, which are part of a central switchboard that mediates the bodys responses to stress and stress-related disorders.
In Alzheimer's disease, as well as various other neurodegenerative conditions, phosphate groups are attached to tau protein, as a result of which the protein looses its grip on the microtubules, and starts to collapse into insoluble protein fibers, which ultimately cause cell death.
Previous studies had shown that extreme physiological stress, such as plunging mice into ice water or starving them for three days, can induce tau phosphorylation.
But what we wanted to know was whether exposure to milder stress, of the kind we experience in our daily lives, can induce tau phosphorylation, explains senior research associate and first author Dr. Robert A. Rissman.
When the researchers restrained mice for half an hour, it resulted only in a transient phosphorylation of tau. But when
they simulated chronic stress by repeating the procedure every day for two weeks, the modification lasted long enough to let tau molecules tumble off the cytoskeleton and pile up in insoluble heaps of protein.
During the study, the researchers genetically engineered mice to lack either CRFR1 or CRFR2.
And sure enough, the CRF receptors turn out to be integrally and differentially involved, says Sawchenko.
In the absence of CRFR1, stress-induced tau phosphorylation was abrogated, while in mice missing CRFR2 the effect was amplified, says the researcher, adding that pharmacological studies with small molecule inhibitors replicated the effect.
We may have discovered another application. Such drugs could have a prophylactic effect or delay the progression of Alzheimers disease, Sawchenko says.
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