Interesting.
Ranjan KC
Researchers have discovered a way to camouflage microrobots in the body using white blood cells to pass through the blood-brain barrier.
Category: biotech/medical – Page 1,538
PINK1, a gene associated with Parkinson’s disease, is not just responsible for the premature death of dopaminergic neurons, it also plays a key role in the neurogenesis of dopamine neurons throughout life.
Leading biogerontologist João Pedro de Magalhães says that longevity pharmacology has come of age, and discusses rapamycin and Calico.
Summary: Combining neuroimaging data with artificial intelligence technology, researchers have identified a complex network within the brain that comprehends the meaning of spoken sentences.
Source: university of rochester medical center.
Have you ever wondered why you are able to hear a sentence and understand its meaning – given that the same words in a different order would have an entirely different meaning?
Should interest those into links on aging/longevity and neuroscience.
The mammalian center for learning and memory, hippocampus, has a remarkable capacity to generate new neurons throughout life. Newborn neurons are produced by neural stem cells (NSCs) and they are crucial for forming neural circuits required for learning and memory, and mood control. During aging, the number of NSCs declines, leading to decreased neurogenesis and age-associated cognitive decline, anxiety, and depression. Thus, identifying the core molecular machinery responsible for NSC preservation is of fundamental importance if we are to use neurogenesis to halt or reverse hippocampal age-related pathology.
While there are increasing number of tools available to study NSCs and neurogenesis in mouse models, one of the major hurdles in exploring this fundamental biological process in the human brain is the lack of specific NSCs markers amenable for advanced imaging and in vivo analysis. A team of researchers led by Dr. Mirjana Maletić-Savatić, associate professor at Baylor College of Medicine and investigator at the Jan and Dan Duncan Neurological Research Institute at Texas Children’s Hospital, and Dr. Louis Manganas, associate professor at the Stony Brook University, decided to tackle this problem in a rather unusual way. They reasoned that if they could find proteins that are present on the surface of NSCs, then they could eventually make agents to “see” NSCs in the human brain.
“The ultimate goal of our research is to maintain neurogenesis throughout life at the same level as it is in the young brains, to prevent the decline in our cognitive capabilities and reduce the tendency towards mood disorders such as depression, as we age. To do that, however, we first need to better understand this elusive, yet fundamental process in humans. However, we do not have the tools to study this process in live humans and all the knowledge we have gathered so far comes from analyses of the postmortem brains. And we cannot develop tools to detect this process in people because existing NSC markers are present within cells and unreachable for in vivo visualization,” Maletić-Savatić said. “So, in collaboration with our colleagues from New York and Spain, we undertook this study to find surface markers and then develop tools such as ligands for positron emission tomography (PET) to visualize them using advanced real-time in vivo brain imaging.”
Following on in the vein of my recent topics, this week I am looking at mTOR. A crucial protein that performs the function of an enzyme that is critical for day to day function. There are so many terms and words, subjects and strategies, abound, and so many talk in terms where a basic understanding of the subject is necessary to benefit fully, that I decided to create a kind of library, or resource where you can brush up on all the core fundamentals. Should you stimulate mTOR or seek to restrict it? What will happen if I do? Is this a short term strategy or a lifestyle goal? And what is the real state of the science that underpins it all? These are all questions you, or friends, may have, or even may have heard but been unable to answer fully or concisely, hopefully these will help to reduce those issues. Next week I will be looking at its partner in crime, AMPK, together they exist in balance like a playground see-saw… Until then, have an amazing day…
In this video I will look at what mTOR is and how you can harness it to benefit your objectives. By controlling it we can achieve the balance we need which is to grow muscle to stay fit and strong, but also to not burn out too quickly, so we can live a long healthy life, with a long health span. Maximising anti aging to aid in longevity is delicate balance unique to us all and which varies depending on our current goals and objectives.
By learning how all these systems interrelate and interact, we can find the best pathway for our own personal journey, I hope this video goes some way to helping you chart that path.
If you want to know more about rapamycin which is the mTOR inhibitor mentioned, why not try this video next…
https://youtu.be/mbszWs1JX7c.
As always the links to the studies and information I referenced is below…
Full coverage of the coronavirus outbreak
Germany started cautiously easing restrictions earlier this month. But the spread of more infectious variants of the virus has pushed up cases, prompting concerns that hospitals could soon be overstretched without further curbs.
ROCHESTER, N.Y. (WHEC) — Monroe County Public Health Commissioner Dr. Michael Mendoza Tuesday announced new COVID-19 variants have been found in Monroe County.
Mendoza announced that two cases of the UK variant and a small sample of the California variant were found in Monroe County in some older cases from February.
The research team, led by Todd Lencz, PhD, with Itsik Pe’er, PhD, Tom Maniatis, PhD, and Erin Flaherty, PhD, of Columbia University, carried out a genetic study identifying a single letter change in the DNA code in the PCDHA3 gene that is associated with schizophrenia. The affected gene makes a type of protein called a protocadherin, which generates a cell surface “barcode” required for neurons to recognize, and communicate with, other neurons. They found that the PCDHA3 variant blocks this normal protocadherin function.
The discovery was made possible by the special genetic characteristics of the samples studied by Lencz’s team—patients with schizophrenia and healthy volunteers drawn from the Ashkenazi Jewish population. The Ashkenazi Jewish population represents an important population for study based on its unique history. Just a few hundred individuals who migrated to Eastern Europe less than 1000 years ago are the ancestors of nearly 10 million Ashkenazi Jews today. This lineage, combined with a tradition of marriage within the community, has resulted in a more uniform genetic background in which to identify disease-related variants.
“In addition to our primary findings regarding PCDHA3 and related genes, we were able— due to the unique characteristics of the Ashkenazi population—to replicate several prior findings in schizophrenia despite relatively small sample sizes,” said Lencz, professor in the Institute of Behavioral Science at the Feinstein Institutes. “In our study, we demonstrated this population represents a smart, cost-effective strategy for identifying disease-related genes. Our findings allow us to zero in on a novel aspect of brain development and function in our quest to develop new treatments for schizophrenia.”
It is well established that rare, damaging genetic variants with strong effects contribute to autism. Although individually rare, these variants are collectively common: Clinical genetic testing identifies them in at least 25 percent of autistic people. Studies of these variants have implicated more than 100 genes — and counting — in autism.
Identifying these genes is important — not only for clinical care, but also for advancing our understanding of the neural circuits and processes involved in autism or in its core traits. It creates the opportunity to develop therapies targeted to specific molecular diagnoses. And as we learn more about these genes and the consequences of variants that disrupt their function, we have the potential to better understand the mechanisms underlying cases of autism in which a definitive genetic diagnosis cannot yet be made.
But the genetic findings in people with autism are not unique; deleterious variants in the same genes are also implicated in other neurodevelopmental conditions, such as intellectual disability, epilepsy, attention deficit hyperactivity disorder and schizophrenia. Specific genes and variants do not map neatly onto categorical clinical diagnoses or the core cognitive and behavioral traits that define them. In fact, there is not yet a single example of a gene that, when mutated, increases the likelihood of autism but not of other neurodevelopmental conditions.