Study in fruitflies strengthens connection among protein misfolding, sleep loss, and age

February 20, 2014
Study in fruitflies strengthens connection among protein misfolding, sleep loss, and age
This is a sleepy fruitfly. Credit: Jini Naidoo, Ph.D., Perelman School of Medicine

Pulling an "all-nighter" before a big test is practically a rite of passage in college. Usually, it's no problem: You stay up all night, take the test, and then crash, rapidly catching up on lost sleep. But as we age, sleep patterns change, and our ability to recoup lost sleep diminishes.

Researchers at the Perelman School of Medicine, University of Pennsylvania, have been studying the molecular mechanisms underpinning sleep. Now they report that the pathways of aging and sleep intersect at the circuitry of a cellular stress response pathway, and that by tinkering with those connections, it may be possible to alter in the aged for the better – at least in fruit flies.

Nirinjini Naidoo, PhD, associate professor in the Center for Sleep and Circadian Neurobiology and the Division of Sleep Medicine, led the study with postdoctoral fellow Marishka Brown, PhD, which was published online before print in the journal Neurobiology of Aging.

Increasing age is well known to disrupt sleep patterns in all sorts of ways. Elderly people sleep at night less than their younger counterparts and also sleep less well. Older individuals also tend to nap more during the day. Naidoo's lab previously reported that aging is associated with increasing levels of protein unfolding, a hallmark of cellular stress called the "unfolded protein response."

Protein misfolding is also a characteristic of several age-related neurodegenerative diseases, such as Alzheimer's and Parkinson's diseases, and as it turns out, also associated with . Naidoo and her team wanted to know if rescuing proper protein folding behavior might counter some of the detrimental sleep patterns in elderly individuals.

Using a video monitoring system to compare the of "young" (9

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JVK
not rated yet Feb 20, 2014
If protein folding is nutrient-dependent and pheromone-controlled in ecologically adapted species from microbes to man, nutrient stress and social stress would contribute to mutations that perturb protein folding, which are associated with physical and mental disorders linked to the sense of smell via the decline in olfactory acuity and specificity that occurs with age in humans.

If mutation-driven evolution occurs, ecological variation and adaptation via ecological, social, neurogenic, and socio-cognitive niche construction probably has nothing to do with physical and mental disorders. That means we can eat what we want, and it will make no difference to our health or to the health of our ancestors. However, experimental evidence suggests that's not true. It also suggests that mutation-driven evolution is a lie for the same reasons.

Ecological adaptations are biophysically constrained, constraint-breaking mutations are probably not beneficial since they perturb protein-folding.
katesisco
not rated yet Feb 23, 2014
Then it all comes down to the fact that we are only capable of surviving in a low-stress environment. Because a high stress environment changes all life even the plants, ergo all the life that depends on plants.
Our high population is a response to stress, and why this environmental stress that is dysfunctional to all life? Our sun, Sol, is a dying magnatar, which through its periodic expenditures of energy, blast the Earth with radiation and magnetism, and heat the core which releases radiation in the form of toxic gases like radon. Our history here is merely adjustment to lesser lethal amounts of radiation, ergo high population.

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