EurekAlert! is packing in the interesting releases today, starting with more on recent research into the age-related decline of mechanisms that clear out the protein aggregates associated with neurodegeneration. Take a look:

Scientists discover age-regulated cellular activities that protect against protein aggregation:

Now, we want to use this mechanistic information to discover the macromolecular basis for these activities and to discover small molecules that will delay the aging program and thus delay the onset of proteotoxicity associated with these diseases by modulating aggregation and disaggregation activities. The hope is that, by manipulating the protective mechanism inherent in cells, we can find a single entity - a single drug - that would be useful for a variety of neurodegenerative diseases where protein aggregation leads to neurodegeneration.

That is a hopeful destination for any research: to uncover sufficent simplicity in the midst of complex biochemistry to build a cost-effective intervention that has widespread utility.

Wear and tear of stress: the psychoneurobiology of aging:

Cumulative stress effects, said McEwen, are showing up in people who are under constant stress, like those in caregiver situations or those who suffer from obesity and/or diabetes. These people are more likely to have decreased telomerase activity. Telomeres are enzymes that regulate how many times an individual cell can divide. Telomeric sequences shorten each time the DNA replicates, which is a process that happens prior to cells dividing. When at least some of the telomeres reach a critically short length, the cell stops dividing and ages (senesces) which may cause or contribute to some age-related diseases.

...

In another review of the current literature on the interactions of the brain, stress and the endocrine system, more evidence shows how cumulative stress and the occurrence of disease may define age more than chronological aging. According to the review, certain diseases start to occur when the anabolic hormone levels start to decrease – when the tissue builders like growth hormones, testosterone, estrogen and thyroid functions start to drop off and when the catabolic hormones start to increase. These hormones, the tissue fuelers, can become too active and actually break the body down. Cortisol – a stress hormone – can become more reactive when responding to acute challenges as one gets older.

This one seems to me to be a good example of people who have a portion of the entire picture to hand, but aren't quite getting the full view - or are applying their incomplete knowledge as a way of explaining the whole problem. Give someone a hammer and everything will be treated as a nail until proven otherwise. Chronic stress is clearly not good for you, but the vital, missing part of the picture here is the accumulation of cellular damage through many other causes.

Exercise helps sustain mental activity as we age, may prevent dementia-like illnesses:

From this review we have found that physical and aerobic exercise training can lower the risk for developing some undesirable age-related changes in cognitive and brain functions, and also help the brain maintain its plasticity - ability to cover one function if another starts failing later in life.

Exercise is very good for you. There's nothing out there today that beats out the proven beneficial effects of moderate exercise combined with calorie restriction for most folk. Take better care of your health, and you'll live a longer life - not to mention increasing your chances of living into an era of real, working anti-aging medicine.

New method shows that neocortical nerve cells are not renewed:

Most bodily organs continually die and regrow a little at a time. It takes two years, for example, for all the cells of the liver to be replaced by fresh ones. Research from Karolinska Institutet in Sweden now shows that there is one important exception to this – the nerve cells of the brain remain the same throughout a person's life.

Many scientists have suspected that the cerebral nerve cells lack this renewal ability. However, studies on apes and rodents have indicated that brain cells can reform in mammals after all – including man. One problem with these findings has been the research methodology, as the most common way of measuring the age of nerve cells is extremely complicated, especially in man, and gives unreliable and controversial results.

You might other past articles on the art and science of pinning an age on different cell populations in the body. It seems the back and forth as to whether we grow new neurons or not is heading back to its original position after some years of results indicating we do. Advances in biotechnology will likely render this all moot - researchers are already closing in on the first therapies that will grow new neurons for therapeutic purposes.

Technorati tags: aging, medical research, science

Posted by Reason at August 11, 2006 7:48 PM | TrackBack (2)