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Practical Wisdom: The Right Way to Do the Right Thing

Barry Schwartz

Fantastic read on how to cultivate practical wisdom on our everyday lives and why it matters in our individual and collective happiness

bookpickings:

Practical Wisdom: The Right Way to Do the Right Thing

Barry Schwartz

Fantastic read on how to cultivate practical wisdom on our everyday lives and why it matters in our individual and collective happiness

Scientists explain how memories stick together

neurosciencestuff:

Scientists at the Salk Institute have created a new model of memory that explains how neurons retain select memories a few hours after an event.

image

This new framework provides a more complete picture of how memory works, which can inform research into disorders liked Parkinson’s, Alzheimer’s,…

(Source: salk.edu)

explore-blog:

Bibo, wonderful animated short film about a lonely robot, a year in the making – a sort of modern-day, sadder version of Pixar’s groundbreaking 1986 classic Luxo Jr.

neurosciencestuff:

Existence of new neuron repair pathway discovered
Most of your neurons can’t be replaced.
Other parts of your body – such as skin and bone – can be replaced by the body growing new cells, but when you injure your neurons, you can’t just grow new ones; instead, the existing cells have to repair themselves.
In the case of axon injury, the neuron is able to repair or sometimes even fully regenerate its axon. But neurons have two sides – the axon (which sends signals to other cells) and the dendrite (which receives signals from other cells).
Melissa Rolls, an associate professor of biochemistry and molecular biology at Penn State and director of the Huck Institutes’ Center for Cellular Dynamics, has done extensive comparisons of axons and dendrites – culminating recently in a paper published in Cell Reports.
“We know that the axon side can repair itself,” says Rolls, “and we know a bunch of the molecular players. But we really didn’t know whether neurons have the same capacity to regenerate their dendrites, and so that’s what we set out to find in this study.”
“Our lab uses a Drosophila model system, where the dendrites are very accessible to manipulation,” she says, “so we decided that we would start by removing all the dendrites from the neurons to see if they could regenerate. We didn’t start with anything subtle, like taking off just a few dendrites. We said ‘Let’s just push the system to its maximum and see if this is even possible.’ And we were surprised because we found that not only is it possible, it’s actually much faster than axon regeneration: at least in the cells that we’re using, axon regeneration takes a day or two to initiate, while dendrite regeneration typically initiates within four to six hours and it works really well. All the cells where we removed the dendrites grew new dendrites – none of them died; so it’s clear that these cells have a way to both detect dendrite injury and initiate regrowth of the injured part.”
Read more

neurosciencestuff:

Existence of new neuron repair pathway discovered

Most of your neurons can’t be replaced.

Other parts of your body – such as skin and bone – can be replaced by the body growing new cells, but when you injure your neurons, you can’t just grow new ones; instead, the existing cells have to repair themselves.

In the case of axon injury, the neuron is able to repair or sometimes even fully regenerate its axon. But neurons have two sides – the axon (which sends signals to other cells) and the dendrite (which receives signals from other cells).

Melissa Rolls, an associate professor of biochemistry and molecular biology at Penn State and director of the Huck Institutes’ Center for Cellular Dynamics, has done extensive comparisons of axons and dendrites – culminating recently in a paper published in Cell Reports.

“We know that the axon side can repair itself,” says Rolls, “and we know a bunch of the molecular players. But we really didn’t know whether neurons have the same capacity to regenerate their dendrites, and so that’s what we set out to find in this study.”

“Our lab uses a Drosophila model system, where the dendrites are very accessible to manipulation,” she says, “so we decided that we would start by removing all the dendrites from the neurons to see if they could regenerate. We didn’t start with anything subtle, like taking off just a few dendrites. We said ‘Let’s just push the system to its maximum and see if this is even possible.’ And we were surprised because we found that not only is it possible, it’s actually much faster than axon regeneration: at least in the cells that we’re using, axon regeneration takes a day or two to initiate, while dendrite regeneration typically initiates within four to six hours and it works really well. All the cells where we removed the dendrites grew new dendrites – none of them died; so it’s clear that these cells have a way to both detect dendrite injury and initiate regrowth of the injured part.”

Read more

neurosciencestuff:

Study provides new insight into how toddlers learn verbs
Parents can help toddlers’ language skills by showing them a variety of examples of different actions, according to new research from the University of Liverpool.
Previous research has shown that verbs pose particular difficulties to toddlers as they refer to actions rather than objects, and actions are often different each time a child sees them.
To find out more about this area of child language, University psychologists asked a group of toddlers to watch one of two short videos.
They then examined whether watching a cartoon star repeat the same action, compared to a character performing three different actions, affected the children’s understanding of verbs.
Developmental psychologist, Dr Katherine Twomey, said: “Knowledge of how children start to learn language is important to our understanding of how they progress throughout preschool and school years.
“This is the first study to indicate that showing toddlers similar but, importantly, not identical actions actually helped them understand what a verb refers to, instead of confusing them as you might expect.”
Dr Jessica Horst from the University of Sussex who collaborated on the research added: “It is a crucial first step in understanding how what children see affects how they learn verbs and action categories, and provides the groundwork for future studies to examine in more detail exactly what kinds of variability affect how children learn words.”

neurosciencestuff:

Study provides new insight into how toddlers learn verbs

Parents can help toddlers’ language skills by showing them a variety of examples of different actions, according to new research from the University of Liverpool.

Previous research has shown that verbs pose particular difficulties to toddlers as they refer to actions rather than objects, and actions are often different each time a child sees them.

To find out more about this area of child language, University psychologists asked a group of toddlers to watch one of two short videos.

They then examined whether watching a cartoon star repeat the same action, compared to a character performing three different actions, affected the children’s understanding of verbs.

Developmental psychologist, Dr Katherine Twomey, said: “Knowledge of how children start to learn language is important to our understanding of how they progress throughout preschool and school years.

“This is the first study to indicate that showing toddlers similar but, importantly, not identical actions actually helped them understand what a verb refers to, instead of confusing them as you might expect.”

Dr Jessica Horst from the University of Sussex who collaborated on the research added: “It is a crucial first step in understanding how what children see affects how they learn verbs and action categories, and provides the groundwork for future studies to examine in more detail exactly what kinds of variability affect how children learn words.”

neurosciencestuff:

Study finds modified stem cells offer potential pathway to treat Alzheimer’s disease
UC Irvine neurobiologists have found that genetically modified neural stem cells show positive results when transplanted into the brains of mice with the symptoms and pathology of Alzheimer’s disease. The pre-clinical trial is published in the journal Stem Cells Research and Therapy, and the approach has been shown to work in two different mouse models.
Alzheimer’s disease, one of the most common forms of dementia, is associated with accumulation of the protein amyloid-beta in the brain in the form of plaques. While the search continues for a viable treatment, scientists are now looking into non-pharmaceutical ways to slow onset of this disease.
One option being considered is increasing the production of the enzyme neprilysin, which breaks down amyloid-beta, and shows lower activity in the brains of people with Alzheimer’s disease. Researchers from UC Irvine investigated the potential of decreasing amyloid-beta by delivering neprilysin to mice brains.
“Studies suggest that neprilysin decreases with age and may therefore influence the risk of Alzheimer’s disease,” said Mathew Blurton-Jones, an assistant professor of neurobiology & behavior. “If amyloid accumulation is the driving cause of Alzheimer’s disease, then therapies that either decrease amyloid-beta production or increase its degradation could be beneficial, especially if they are started early enough.”
The brain is protected by a system called the blood-brain-barrier that restricts access of cells, proteins, and drugs to the brain. While the blood-brain-barrier is important for brain health, it also makes it challenging to deliver therapeutic proteins or drugs to the brain. To overcome this, the researchers hypothesized that stem cells could act as an effective delivery vehicle. To test this hypothesis the brains of two different mouse models (3xTg-AD and Thy1-APP) were injected with genetically modified neural stem cells that over-expressed neprilysin.
These genetically modified stem cells were found to produce 25-times more neprilysin than control neural stem cells, but were otherwise equivalent to the control cells. The genetically modified and control stem cells were then transplanted into the hippocampus or subiculum of the mice brains – two areas of the brain that are greatly affected by Alzheimer’s disease. The mice transplanted with genetically modified stem cells were found to have a significant reduction in amyloid-beta plaques within their brains compared to the controls. The effect remained even one month after stem cell transplantation. This new approach could provide a significant advantage over unmodified neural stem cells because neprilysin-expressing cells could not only promote the growth of brain connections but could also target and reduce amyloid-beta pathology.
Before this can be investigated in humans, more work needs to be done to see if this affects the accumulation of soluble forms of amyloid-beta. Further investigation is also needed to determine whether this new approach improves cognition more than the transplantation of un-modified neural stem cells.
“Every mouse model of Alzheimer’s disease is different and develops varying amounts, distribution, and types of amyloid-beta pathology,” Blurton-Jones said. “By studying the same question in two independent transgenic models, we can increase our confidence that these results are meaningful and applicable to Alzheimer’s disease. But there is clearly a great deal more research needed to determine whether this kind of approach could eventually be translated to the clinic.”

neurosciencestuff:

Study finds modified stem cells offer potential pathway to treat Alzheimer’s disease

UC Irvine neurobiologists have found that genetically modified neural stem cells show positive results when transplanted into the brains of mice with the symptoms and pathology of Alzheimer’s disease. The pre-clinical trial is published in the journal Stem Cells Research and Therapy, and the approach has been shown to work in two different mouse models.

Alzheimer’s disease, one of the most common forms of dementia, is associated with accumulation of the protein amyloid-beta in the brain in the form of plaques. While the search continues for a viable treatment, scientists are now looking into non-pharmaceutical ways to slow onset of this disease.

One option being considered is increasing the production of the enzyme neprilysin, which breaks down amyloid-beta, and shows lower activity in the brains of people with Alzheimer’s disease. Researchers from UC Irvine investigated the potential of decreasing amyloid-beta by delivering neprilysin to mice brains.

“Studies suggest that neprilysin decreases with age and may therefore influence the risk of Alzheimer’s disease,” said Mathew Blurton-Jones, an assistant professor of neurobiology & behavior. “If amyloid accumulation is the driving cause of Alzheimer’s disease, then therapies that either decrease amyloid-beta production or increase its degradation could be beneficial, especially if they are started early enough.”

The brain is protected by a system called the blood-brain-barrier that restricts access of cells, proteins, and drugs to the brain. While the blood-brain-barrier is important for brain health, it also makes it challenging to deliver therapeutic proteins or drugs to the brain. To overcome this, the researchers hypothesized that stem cells could act as an effective delivery vehicle. To test this hypothesis the brains of two different mouse models (3xTg-AD and Thy1-APP) were injected with genetically modified neural stem cells that over-expressed neprilysin.

These genetically modified stem cells were found to produce 25-times more neprilysin than control neural stem cells, but were otherwise equivalent to the control cells. The genetically modified and control stem cells were then transplanted into the hippocampus or subiculum of the mice brains – two areas of the brain that are greatly affected by Alzheimer’s disease. The mice transplanted with genetically modified stem cells were found to have a significant reduction in amyloid-beta plaques within their brains compared to the controls. The effect remained even one month after stem cell transplantation. This new approach could provide a significant advantage over unmodified neural stem cells because neprilysin-expressing cells could not only promote the growth of brain connections but could also target and reduce amyloid-beta pathology.

Before this can be investigated in humans, more work needs to be done to see if this affects the accumulation of soluble forms of amyloid-beta. Further investigation is also needed to determine whether this new approach improves cognition more than the transplantation of un-modified neural stem cells.

“Every mouse model of Alzheimer’s disease is different and develops varying amounts, distribution, and types of amyloid-beta pathology,” Blurton-Jones said. “By studying the same question in two independent transgenic models, we can increase our confidence that these results are meaningful and applicable to Alzheimer’s disease. But there is clearly a great deal more research needed to determine whether this kind of approach could eventually be translated to the clinic.”