Another rat plasma experiment, and it’s all good.
Key points summary of Live Forever Club article. 2 month life extension is equivalent of giving a 60 year-old human an extra 6 years of healthy life.
Brains are like puzzles, requiring many nested and co-dependent pieces to function well. The brain is divided into areas, each containing many millions of neurons connected across thousands of synapses. These synapses, which enable communication between neurons, depend on even smaller structures: message-sending boutons (swollen bulbs at the branch-like tips of neurons), message-receiving dendrites (complementary branch-like structures for receiving bouton messages), and power-generating mitochondria. To create a cohesive brain, all these pieces must be accounted for.
However, in the aging brain, these pieces can get lost or altered, and no longer fit in the greater brain puzzle. A research team has now published a study in Frontiers in Aging Neuroscience on this topic.
“Fifty percent of people experience loss of working memory with old age, meaning their ability to hold and manipulate information in the short-term decreases,” says co-first author Courtney Glavis-Bloom, a senior staff scientist in Salk Institute Professor John Reynolds’s lab. “We set out to understand why some individuals maintain healthy working memory as they age, while others do not. In the process, we discovered a novel mechanism for the synaptic basis of cognitive impairment.”
A new study in both mice and humans has found that biological age is dynamic, and that some increases in biological age caused by stress can be reversed with recovery. The research is published in Cell Metab olism.
How can we measure age?
Our biological age is not completely linked to our chronological age. While chronological age is a measure of the amount of time you have been alive, biological age indicates how much aging has occurred to your cells over your lifetime.
Wake Forest Institute for Regenerative Medicine (WFIRM) scientists have created a promising injectable cell therapy to treat osteoarthritis that both reduces inflammation and also regenerates articular cartilage.
Recently identified by the Food and Drug Administration as a public health crisis, osteoarthritis affects more than 520 million people worldwide who deal with pain and inflammation. Osteoarthritis is typically induced by mechanical or traumatic stress in the joint, leading to damaged cartilage that cannot be repaired naturally.
“Without better understanding of what drives the initiation and progression of osteoarthritis, effective treatment has been limited,” said lead author Johanna Bolander of WFIRM. “Initially, we studied what goes wrong in osteoarthritic joints, compared these processes to functional environments, and used this information to develop an immunotherapy cell treatment.”
At last, a new study has found the answers to “basic biology questions” that could help explain what drives ageing and what can we do to reverse it.
Calorie restriction, a proven intervention to slow aging in animals, showed evidence of slowing the pace of biological aging in a human randomized trial.
In a first-of-its-kind randomized controlled trial, an international team of researchers led by the Columbia Aging Center at Columbia University.
Columbia University is a private Ivy League research university in New York City that was established in 1754. This makes it the oldest institution of higher education in New York and the fifth-oldest in the United States. It is often just referred to as Columbia, but its official name is Columbia University in the City of New York.
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Summary: Listening to or practicing music had positive implications on cognitive decline in older adults by stimulating the production of gray matter in key brain areas, a new study reveals.
Source: University of Geneva.
Normal aging is associated with progressive cognitive decline. But can we train our brain to delay this process?
Researchers at UC Davis are the first to report how a specific type of brain cells, known as oligodendrocyte-lineage cells, transfer cell material to neurons in the mouse brain. Their work provides evidence of a coordinated nuclear interaction between these cells and neurons. The study was published today in the Journal of Experimental Medicine.
“This novel concept of material transfer to neurons opens new possibilities for understanding brain maturation and finding treatments for neurological conditions, such as Alzheimer’s disease, cerebral palsy, Parkinson’s and Huntington’s disease,” said corresponding author Olga Chechneva is an assistant project scientist at UC Davis Department of Biochemistry and Molecular Medicine and independent principal investigator in the Institute for Pediatric Regenerative Medicine at Shriners Children’s Northern California.
Oligodendrocyte-lineage cells, also called oligodendroglia, are a type of glial cells found in the central nervous system. From birth onward, these glial cells arise to support neural circuit maturation. They are mostly known for their role in myelination—the formation of the insulating myelin sheath around nerve axons.
Senescent cells are those that have stopped dividing but haven’t read the “time to die” memo. Instead, they hang around, accumulating in the body and fueling chronic inflammation – sometimes called inflammaging – which in turn, contributes to conditions such cardiovascular diseases, chronic kidney disease, type 2 diabetes, cancer, sarcopenia and degenerative disorders.
Longevity. Technology: In mice, eliminating senescent cells from aging tissues can restore tissue balance and lead to an increased healthy lifespan. Now a team led by investigators at Massachusetts General Hospital (MGH), a founding member of Mass General Brigham (MGB), has found that the immune response to a virus that is ubiquitously present in human tissues can detect and eliminate senescent cells in the skin [1].
For the study, which is published in Cell, the scientists analyzed young and old human skin samples to learn more about the clearance of senescent cells in human tissue.
