If you’re 18 right now, you think you invented platform shoes. You think you’re doing something new. You think you’ve invented something so ugly that it’s beautiful. When we were young, we knew things. We knew basic history, even as it related to fashion. Now, when something reappears, an 18 year old has no clue that it’s a revival. Despite the fact that they’re almost always online they don’t get references. I think that’s part of why visual things are becoming so derivative. Designers now, they all have these things called mood boards. I suppose they think a sense of discovery equals invention. It would be as if every writer had a board with paragraphs of other writers—’Oh, I’ll take a little bit of this, and that, he was really good.’ Yes, he was really good! And that is not a mood board, it is a stealing board.
—  Fran Lebowitz being delightfully cranky. (As for the stealing board, good idea, I think Phil Pullman would call that “reading.”) Like she says in her Paris Review interview, “I wouldn’t say that I dislike the young. I’m simply not a fan of naïveté.” Fun to compare with Bill Cunningham, who has 20 years on her, on seeing a youthful art show: “It gave me the greatest hope for our civilization.” I liked later in the interview, where she makes fun of young people for having a good relationship with their parents. (“Our parents weren’t our friends. They disapproved of us.”) Reminded me of Stafford Beer: “If we can understand our children, we’re all screwed.”

Even at a molecular level, taking it slow helps us cope with stress

UC Berkeley scientists have identified a new molecular pathway critical to aging, and confirmed that the process can be manipulated to help make old blood like new again.

The researchers found that blood stem cells’ ability to repair damage caused by inappropriate protein folding in the mitochondria, a cell’s energy station, is critical to their survival and regenerative capacity.

The discovery, to be published in the March 20 issue of the journal Science, has implications for research on reversing the signs of aging, a process thought to be caused by increased cellular stress and damage.

“Ultimately, a cell dies when it can’t deal well with stress,” said study senior author Danica Chen, an assistant professor in the Department of Nutritional Sciences and Toxicology. “We found that by slowing down the activity of mitochondria in the blood stem cells of mice, we were able to enhance their capacity to handle stress and rejuvenate old blood. This confirms the significance of this pathway in the aging process.”

Mitochondria host a multitude of proteins that need to be folded properly to function correctly. When the folding goes awry, the mitochondrial unfolded-protein response, or UPRmt, kicks in to boost the production of specific proteins to fix or remove the misfolded protein.

Chen’s lab stumbled upon the importance of UPRmt in blood stem cell aging while studying a class of proteins known as sirtuins, which are increasingly recognized as stress-resistance regulators.

The researchers noticed that levels of one particular sirtuin, SIRT7, increase as a way to help cells cope with stress from misfolded proteins in the mitochondria. Notably, SIRT7 levels decline with age.

There has been little research on the UPRmt pathway, but studies in roundworms suggest that its activity increases when there is a burst of mitochondrial growth.

Chen noted that adult stem cells are normally in a quiescent, standby mode with little mitochondrial activity. They are activated only when needed to replenish tissue, at which time mitochondrial activity increases and stem cells proliferate and differentiate. When protein-folding problems occur, however, this fast growth could lead to more harm.

“We isolated blood stem cells from aged mice and found that when we increased the levels of SIRT7, we were able to reduce mitochondrial protein-folding stress,” said Chen. “We then transplanted the blood stem cells back into mice, and SIRT7 improved the blood stem cells’ regenerative capacity.”

The new study found that blood stem cells deficient in SIRT7 proliferate more. This faster growth is due to increased protein production and increased activity of the mitochondria, and slowing things down appears to be a critical step in giving cells time to recover from stress, the researchers found. Chen likened this to an auto accident or stalled car jamming traffic on a freeway.

“You can deal with this congestion by removing all the cars that are blocked, but you can also stop more cars from getting onto the freeway,” she said. “When there’s a mitochondrial protein-folding problem, there is a traffic jam in the mitochondria. If you prevent more proteins from being created and added to the mitochondria, you are helping to reduce the jam.”

Until this study, it was unclear which stress signals regulate the transition of stem cells to and from the quiescent mode, and how that related to tissue regeneration during aging.

“Identifying the role of this mitochondrial pathway in blood stem cells gives us a new target for controlling the aging process,” said Chen.

The rise and fall of cognitive skills

Scientists have long known that our ability to think quickly and recall information, also known as fluid intelligence, peaks around age 20 and then begins a slow decline. However, more recent findings, including a new study from neuroscientists at MIT and Massachusetts General Hospital (MGH), suggest that the real picture is much more complex.

The study, which appears in the journal Psychological Science, finds that different components of fluid intelligence peak at different ages, some as late as age 40.

“At any given age, you’re getting better at some things, you’re getting worse at some other things, and you’re at a plateau at some other things. There’s probably not one age at which you’re peak on most things, much less all of them,” says Joshua Hartshorne, a postdoc in MIT’s Department of Brain and Cognitive Sciences and one of the paper’s authors.

“It paints a different picture of the way we change over the lifespan than psychology and neuroscience have traditionally painted,” adds Laura Germine, a postdoc in psychiatric and neurodevelopmental genetics at MGH and the paper’s other author.

Measuring peaks

Until now, it has been difficult to study how cognitive skills change over time because of the challenge of getting large numbers of people older than college students and younger than 65 to come to a psychology laboratory to participate in experiments. Hartshorne and Germine were able to take a broader look at aging and cognition because they have been running large-scale experiments on the Internet, where people of any age can become research subjects.

Their web sites, gameswithwords.org and testmybrain.org, feature cognitive tests designed to be completed in just a few minutes. Through these sites, the researchers have accumulated data from nearly 3 million people in the past several years.

In 2011, Germine published a study showing that the ability to recognize faces improves until the early 30s before gradually starting to decline. This finding did not fit into the theory that fluid intelligence peaks in late adolescence. Around the same time, Hartshorne found that subjects’ performance on a visual short-term memory task also peaked in the early 30s.

Intrigued by these results, the researchers, then graduate students at Harvard University, decided that they needed to explore a different source of data, in case some aspect of collecting data on the Internet was skewing the results. They dug out sets of data, collected decades ago, on adult performance at different ages on the Weschler Adult Intelligence Scale, which is used to measure IQ, and the Weschler Memory Scale. Together, these tests measure about 30 different subsets of intelligence, such as digit memorization, visual search, and assembling puzzles.

Hartshorne and Germine developed a new way to analyze the data that allowed them to compare the age peaks for each task. “We were mapping when these cognitive abilities were peaking, and we saw there was no single peak for all abilities. The peaks were all over the place,” Hartshorne says. “This was the smoking gun.”

However, the dataset was not as large as the researchers would have liked, so they decided to test several of the same cognitive skills with their larger pools of Internet study participants. For the Internet study, the researchers chose four tasks that peaked at different ages, based on the data from the Weschler tests. They also included a test of the ability to perceive others’ emotional state, which is not measured by the Weschler tests.

The researchers gathered data from nearly 50,000 subjects and found a very clear picture showing that each cognitive skill they were testing peaked at a different age. For example, raw speed in processing information appears to peak around age 18 or 19, then immediately starts to decline. Meanwhile, short-term memory continues to improve until around age 25, when it levels off and then begins to drop around age 35.

For the ability to evaluate other people’s emotional states, the peak occurred much later, in the 40s or 50s.

Christopher Chabris, an associate professor of psychology at Union College, said a key feature of the study’s success was the researchers’ ability to gather and analyze so much data, which is unusual in cognitive psychology.

“You need to look at a lot of people to discover these patterns,” says Chabris, who was not part of the research team. “They’re taking the next step and showing a more fine-grained picture of how cognitive abilities differ from one another and the way they change over time.”

More work will be needed to reveal why each of these skills peaks at different times, the researchers say. However, previous studies have hinted that genetic changes or changes in brain structure may play a role.

“If you go into the data on gene expression or brain structure at different ages, you see these lifespan patterns that we don’t know what to make of. The brain seems to continue to change in dynamic ways through early adulthood and middle age,” Germine says. “The question is: What does it mean? How does it map onto the way you function in the world, or the way you think, or the way you change as you age?”

Accumulated intelligence

The researchers also included a vocabulary test, which serves as a measure of what is known as crystallized intelligence — the accumulation of facts and knowledge. These results confirmed that crystallized intelligence peaks later in life, as previously believed, but the researchers also found something unexpected: While data from the Weschler IQ tests suggested that vocabulary peaks in the late 40s, the new data showed a later peak, in the late 60s or early 70s.

The researchers believe this may be a result of better education, more people having jobs that require a lot of reading, and more opportunities for intellectual stimulation for older people.

Hartshorne and Germine are now gathering more data from their websites and have added new cognitive tasks designed to evaluate social and emotional intelligence, language skills, and executive function. They are also working on making their data public so that other researchers can access it and perform other types of studies and analyses.

“We took the existing theories that were out there and showed that they’re all wrong. The question now is: What is the right one? To get to that answer, we’re going to need to run a lot more studies and collect a lot more data,” Hartshorne says.

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A new understanding of Alzheimer’s

Although natural selection is often thought of as a force that determines the adaptation of replicating organisms to their environment, Harvard researchers have found that selection also occurs at the level of neurons, which are post-mitotic cells, and plays a critical role in the emergence of Alzheimer’s disease.

Using the principles of natural selection, Lloyd Demetrius, a researcher in population genetics at Harvard’s Museum of Comparative Zoology, and Jane Driver, an assistant professor of medicine at Harvard Medical School, have proposed a new model of Alzheimer’s that suggests mitochondria — cellular power plants — might be at the center of the disease. The study, which builds on earlier work by Demetrius and David Simon, an associate professor of neurology at HMS, was described in a recent paper in the Journal of the Royal Society Interface.

“We felt that, in order to explain the exponential increase in Alzheimer’s with age, we had to move away from the nuclear genome and look at what is going on with the energy-producing organelles,” Demetrius said. “That led us to a completely different model for the disease. We do not rule out the nuclear genes as playing a role … but, for the late-onset form of Alzheimer’s, we envision a mechanism based on the fact that mitochondrial DNA has a high mutation rate and that the organelles generate less energy with age.”

The prevalent model of Alzheimer’s is known as the amyloid cascade model. Proposed more than two decades ago, the amyloid hypothesis says that Alzheimer’s is primarily driven by the accumulation of beta amyloid in neurons. The accumulation is thought to be triggered by a mutation in the nuclear genome. A number of clinical trials have been conducted based on the model, but none have shown positive results. That prompted Demetrius and Driver to take a hard look at the fundamental underlying assumptions.

“A lot of people are realizing now that we have been focusing on the usual suspects — genetics and proteins ― and that’s brought us to a point where, despite billions of dollars in research, we are no closer to a disease-modifying therapy,” Driver said. “Of course, that’s not to suggest that genetics isn’t important, but I think what we haven’t done is to take the 20,000-foot view and ask if it is even logical to expect that changes to one protein could be responsible for an age-related disease. It just didn’t add up.”

The genetic mutation model could explain early onset Alzheimer’s, but this form of the disease accounts for only about 5 percent of cases.

“The late-onset cases, however, are quite different,” Demetrius said. “They increase exponentially with age, and that is one of the most striking characteristics of the disease. As you age, the chances of getting it increase.”

In the model Demetrius and Driver describe, the disease’s first step is what they call “mitochondrial dysregulation.” The process is largely part of the natural course of aging.

As a person ages, the researchers say, the mitochondria in the cells generate energy less and less efficiently. Mitochondria, with their own DNA, are akin to the descendants of simple organisms that lived in a symbiotic relationship inside more complex ones. The mitochondria that produce cellular energy from nutrients such as glucose, in a process called oxidative phosphorylation, are incredibly efficient.

However, the process has the side effect of producing oxygen-free radicals, which can damage mitochondrial DNA and proteins. Random mutations can further damage mitochondrial structure and function. The accumulated harm leads to an energy deficit, triggering a compensatory event that Demetrius and Driver call “metabolic re-programming” — unaffected mitochondria increase output, by upregulating oxidative phosphorylation, to make up for the energy deficit.

The end result is two broad types of neurons ― relatively healthy, and impaired ― that must compete for nutrients. Impaired neurons, since they contain some mitochondria with upregulated activity, have an advantage in the competition. That competition, Demetrius said, plays out according to the principles of natural selection.

With normal aging, the two populations eventually reach equilibrium, typically with healthy neurons far outnumbering impaired neurons. As long as the balance is maintained, a person won’t slide into the grip of disease.

What can set a person on the path toward Alzheimer’s is the metabolic upheaval that accompanies both physical and emotional stress.

Ailments such as a stroke or a major depression disrupt the neuronal microenvironment and put additional stress on neurons. Some die, and others have to increase their energy production in order to survive. As a result, impaired neurons take up a larger share of the brain’s resources and begin to out-compete healthy neurons for nutrients.

“When that happens, you have a rapid shift toward Alzheimer’s — what I call pathological aging,” Demetrius said. “The two types of neurons are competing with each other, but the impaired neurons, in view of the particular environment of the aging brain, have a selective advantage.”

The healthy neurons die immediately because they are overwhelmed by the impaired neurons. The impaired neurons ultimately die because of the deleterious effects of the reactive oxygen species generated by their upregulated metabolic activity.

Metabolic reprogramming, a cornerstone of the model, is called the Inverse Warburg Effect because it is analogous to the mode of metabolic alteration the Nobel laureate Otto Warburg proposed almost 100 years ago to explain the origin of late-onset forms of cancer. The metabolic shift in this case is the upregulation of glycolysis.

“The therapeutic implications are quite simple,” Demetrius said. “In order to prevent this shift from normal to pathological aging, all we need to do is ensure that the quasi-equilibrium between intact and impaired neurons remains stable, and we can do that through what we call metabolic interventions.”

The treatment involves interventions such as exercise, drugs, or nutrients that alter the neuronal microenviroment so that healthy neurons maintain their selective advantage and the brain doesn’t shift from normal to pathological aging. There is some evidence that increasing the availability of energy precursors such as lactate, ketones, and triglycerides may help neurons facing an energy crisis. Approaches that support the health and function of the astrocytes — the neuron’s metabolic support cells — could also act protectively.

“If you take good care of your blood pressure, if you exercise regularly and eat a lower-calorie diet ― all those things contribute to metabolic health,” Driver said. “The things we need to do to prevent Alzheimer’s, or at least make a dent in the incidence of the disease, are within our hands.”


Aging: ldentifying Puberty in the Osteoarchaeological Record
Source: https://thesebonesofmine.wordpress.com/2015/02/15/aging-ldentifying-puberty-in-the-osteoarchaeological-record/

Aside from some recent technological mishaps (now resolved!), which has resulted in a lack of posts recently, I’ve also been doing some preliminary research into human skeletal aging and human biological aging in general.  Partly this has been out of general interest, but it was also background reading for a small project that I was working on over the past few months. Knowledge of the aging of the skeletal system is of vital importance to the bioarchaeologist as it allows age estimates to be made of both individuals and of populations (and thus estimates of lifespans between generations……….Read More

AN AGE OLD PROBLEM

Pulitzer Center student fellow Michelle Ferng, a Johns Hopkins Global Health Scholar, sheds light on an underreported epidemic: “Older adults worldwide suffering from abuse and abandonment, often by those closest to them. The majority of victims remain hidden from public view. Only rarely do extreme cases command attention.”

In her feature story for the Johns Hopkins Bloomberg School of Public Health magazine, Michelle writes that “one of the most tragic facets of the coming demographic shift is elder abuse, which can take various forms: physical, psychological/ emotional, financial/material and sexual, as well as abandonment or neglect.”

Examining the crisis in Peru, Michelle documents the cases of several older adults who have been left to fend for themselves. It is a surprising problem that appears to be growing across the region. “In many ways, time is running out,” says Michelle. “Between 2000 and 2050, the proportion of the world’s population over 60 years old is projected to double from about 11 to 22 percent, according to the WHO. One million people turn 60 every month, and 80 percent of these are in the developing world.”

Human brains age less than previously thought

Older brains may be more similar to younger brains than previously thought. In a new paper published in Human Brain Mapping, BBSRC-funded researchers at the University of Cambridge and Medical Research Council’s Cognition and Brain Sciences Unit demonstrate that previously reported changes in the ageing brain using functional magnetic resonance imaging (fMRI) may be due to vascular (or blood vessels) changes, rather than changes in neuronal activity itself. Given the large number of fMRI studies used to assess the ageing brain, this has important consequences for understanding how the brain changes with age and challenges current theories of ageing.

A fundamental problem of fMRI is that it measures neural activity indirectly through changes in regional blood flow. Thus, without careful correction for age differences in vasculature reactivity, differences in fMRI signals can be erroneously regarded as neuronal differences. An important line of research focuses on controlling for noise in fMRI signals using additional baseline measures of vascular function. However, such methods have not been widely used, possibly because they are impractical to implement in studies of ageing.

An alternative candidate for correction makes use of resting state fMRI measurements, which is easy to acquire in most fMRI experiments. While this method has been difficult to validate in the past, the unique combination of an impressive data set across 335 healthy volunteers over the lifespan, as part of the CamCAN project, allowed Dr. Kamen Tsvetanov and colleagues to probe the true nature of ageing effects on resting state fMRI signal amplitude. Their research showed that age differences in signal amplitude during a task are of a vascular, not neuronal, origin. They propose that their method can be used as a robust correction factor to control for vascular differences in fMRI studies of ageing.

The study also challenged previous demonstrations of reduced brain activity in visual and auditory areas during simple sensorimotor tasks. Using conventional methods, the current study replicated these findings. However, after correction, Tsvetanov et al. results show that it might be vascular health, not brain function, that accounts for most age-related differences in fMRI signal in sensory areas. Their results suggest that the age differences in brain activity may be overestimated in previous fMRI studies of ageing.

Dr. Tsvetanov said: “There is a need to refine the practice of conducting fMRI. Importantly, this doesn’t mean that studies lacking ‘golden standard’ calibration measures, such as large scale studies, patient studies or ongoing longitudinal studies are invalid. Instead, researchers should make use of available resting state data as a suitable alternative. These findings clearly show that without such correction methods, fMRI studies of the effects of age on cognition may misinterpret effect of age as a cognitive, rather than vascular, phenomena.”