Archived News
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Removal of Aging Cells Could Extend Human Life
Date: 11/06/2017
A recent study, led by an international team of researchers confirms that targeted removal of senescent cells (SnCs), accumulated in many vertebrate tissues as we age, contribute significantly in delaying the onset of age-related pathologies.
This breakthrough research has been led by Dr. Chaekyu Kim of the Johns Hopkins University School of Medicine, who is now at UNIST, and Dr. Ok Hee Jeon of the Johns Hopkins University School of Medicine in collaborations with the Mayo Clinic College of Medicine, the Buck Institute for Research on Aging, the University Medical Center Groningen, Unity Biotechnology, Inc., and the University of California, Berkeley.
In the study, the research team presented a novel pharmacologic candidate that alleviates age-related degenerative joint conditions, such as osteoarthritis (OA) by selectively destroying SnCs. Their findings, published April 24th in Nature Medicine, suggest that the selective removal of old cells from joints could reduce the development of post-traumatic OA and allow new cartilage to grow and repair joints.
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Distinct Wiring Mode Found in Chandelier Cells
Date: 11/06/2017
Researchers at the Max Planck Florida Institute for Neuroscience identify the wiring process of a unique type of inhibitory cells implicated in several diseases.
A basic tenet of neural development is that young neurons make far more connections than they will actually use, with very little specificity. They selectively maintain only the ones that they end up needing. Once many of these connections are made, the brain employs a use-it or lose-it strategy; if the organism’s subsequent experiences stimulate the synapse, it will strengthen and survive. If not, the synapse will weaken and eventually disappear.
Researchers from Hiroki Taniguchi’s lab at the Max Planck Florida Institute for Neuroscience (MPFI) published a study in eNeuro in May 2017 showing for the first time that a unique type of inhibitory interneuron called chandelier cells – which are implicated in several diseases affecting the brain such as schizophrenia and epilepsy – seem to develop their connections differently than other types of neurons.
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Hippocampus Can Organize Memories for Events as Well as Places
Date: 11/06/2017
People organize memories in photo albums, journals or calendars, but how does the brain first put events in order? Though a great deal of work has been done on how the brain encodes memory for locations, leading to the discovery of ‘place cells’ in the hippocampus, we still have relatively little understanding of how personally experienced, or episodic, memories are represented by neurons. Now, researchers at Japan’s RIKEN Brain Science Institute have found that the hippocampus can generalize, putting not just places but also events into sequence by changing the neural code in the rat brain. These ‘event cells’ discovered by the researchers may be a bridge linking information about the world with subsequent decision-making.
Neurons have two main ways they can signal to each other: by changing the timing or the frequency of their firing. In this study, Shigeyoshi Fujisawa and colleagues looked at how these two parameters changed while rats did a decision-making task based on certain combinations of smells and sounds. Using non-spatial stimuli presented in sequence was crucial to demonstrating that cells in the hippocampus also represent events, not just places. The study was published in the journal Neuron on June 8.
The research team recorded the combined activity of a large number of neurons in central hippocampal area CA1 while rats were engaged in choosing different sound-odor combinations to get a water reward. Many cells displayed elevated activity in response to one or both stimuli–often with a strong preference for one odor or sound versus the other–and retained this activation through the ‘decision’ phase, indicating that the inputs were being integrated by the brain and retained in a specific order to facilitate a subsequent choice.
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Gene That Enables Memories and Sense of Direction Produces Schizophrenia Like Symptoms When Mutated
Date: 24/01/2017
Mutations in a gene that should enable memories and a sense of direction instead can result in imprecise communication between neurons that contributes to symptoms of schizophrenia, scientists report.
They found that dramatically reducing the amount of protein expressed by TMEM108, a gene already associated with schizophrenia, results in fewer, smaller spines, which work like communication fingers for neurons, said neuroscientist Dr. Lin Mei.
That translates to an impaired ability for neurons to receive whatever signals surrounding neurons are trying to send and mice displaying schizophrenia-like behavioral deficits such as impaired cognition and sense of direction.
“We knew this gene’s alteration likely contributed to schizophrenia and we wanted to better understand how,” said Mei, chairman of the Department of Neuroscience and Regenerative Medicine at the Medical College of Georgia at Augusta University, Georgia Research Alliance Eminent Scholar in Neuroscience and a corresponding author of the study in the journal PNAS.
While some TMEM108 can be found throughout the central nervous system, it appears to normally cluster in the dentate gyrus, an area in the brain’s hippocampus known to be critical for spatial coding – which literally provides a sense of direction – as well as emotion and the ability to learn and remember, which are all affected in schizophrenia. Dentate gyrus dysfunction also is implicated in psychiatric disorders, including schizophrenia.
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