Jung, Yu, Choi et al. reveal a critical neuroprotective role of PTMS, while loss of this protein causes severe neurodegeneration. Hypothalamic neural stem cell-derived extracellular vesicles carrying PTMS protect neurons by preventing DNA damage and offer therapeutic benefits against aging-related neurodegenerative and Alzheimer’s-like conditions in animal models.
From work meetings to first dates, it’s essential to adjust our behavior for success. In certain situations, it can even be a matter of life or death. So how do we switch our behavior when situations change? Published in Nature Communications, neuroscientists describe the neural basis of behavioral flexibility in mice, with insights which may help us understand a wide variety of diseases and disorders, from addiction to obsessive compulsive disorder (OCD) to Parkinson’s disease.
“The brain mechanisms behind changing behaviors have remained elusive, because adapting to a given scenario is very neurologically complex. It requires interconnected activity across multiple areas of the brain,” explains a co-author. “Previous work has indicated that cholinergic interneurons—brain cells that release a neurotransmitter called acetylcholine—are involved in enabling behavioral flexibility. Here, we were able to use advanced imaging techniques to see neurotransmitter release in real time and delve into the fundamental mechanisms behind behavioral flexibility”
In their investigations, the researchers trained mice in a virtual maze, teaching them the correct route to receive a reward. They then switched the route, leading to an unexpected loss of reward for the mice, and observed the effects of this disappointing change using two-photon microscopy.
Yale School of Medicine (YSM) scientists have discovered a molecular difference in the brains of autistic people compared to their neurotypical counterparts.
Autism is a neurodevelopmental condition associated with behavioral differences including difficulties with social interaction, restrictive or intense interests, and repetitive movements or speech. But it’s not clear what makes autistic brains different.
Now, a study in the American Journal of Psychiatry has found that the brains of autistic people have fewer of a specific kind of receptor for glutamate, the most common excitatory neurotransmitter in the brain. The reduced availability of these receptors may be associated with various characteristics linked to autism.
The Fine-Tuning Argument is often seen as the best argument for the existence of God. Here we have assembled some of the world’s top physicists and philosophers to offer a reply. Not every critic of the argument comes from the same perspective. Some doubt there is a problem to be solved whilst others agree it is a genuine problem but think there are better solutions than the God hypothesis. Some like the multiverse and anthropics other don’t. We have tried to represent these different approaches and so it should be taken as given, that not all of the talking heads agree with each other. Nevertheless, they all share the view that the fine-tuning argument for God does not work. Nor are all the objectors atheist, Hans Halvorson offers what we think is a strong theological objection to the argument. This film does not try to argue that God doesn’t exist only that the fine-tuning argument is not a good reason to believe in God. Most of the footage was filmed exclusively for this film with some clips being re-used from our Before the Big Bang series, which can be viewed here: • Before the Big Bang 5: The No Boundary Pro… All of the critics of the fine tuning argument that appear were sent a draft of the film more than a month before release and asked for any objections either to their appearance, the narration or any other aspect of the film. No objections were raised, and many replies were extremely positive and encouraging. A timeline of the subjects covered is below:
(We define God as a perfect Omni immaterial mind as for example modern Christians and Muslims advocate, there are other conceptions of God which our video does not address).
Just to be clear, this is a polemical film arguing against the fine tuning argument.
Timecodes.
0:00 Introduction.
4:11 The universe as a roll of the dice.
6:15 what is probability?
7:28 probability problems.
9:25 measure problem.
15:45 deceptive probabilities.
20:23 the flatness problem.
22:14 counterfactuals versus probabilities.
23:59 fine tuning versus God.
37:02 necessity.
38:53 multiverse and anthropics.
47:34 Boltzmann brains.
49:45 Entropy.
52:45 Cosmological Natural Selection.
59:10 conclusion.
More than 7 million Americans have Alzheimer’s disease, and two-thirds of them are women, according to the Alzheimer’s Association. The O’Banion Lab at the Del Monte Institute for Neuroscience at the University of Rochester has long been studying this disease and is looking more closely at the differences between male and female brains.
“It is well documented that males and females are diagnosed with Alzheimer’s disease at different rates,” said M. Kerry O’Banion, MD, Ph.D., professor of Neuroscience and Neurology. “But we still do not have a great understanding of why this is the case. We can only improve any possible treatment or prevention of this disease if we know the why, when, and where these differences are occurring.”
A designer version of the tau protein, developed by a team led by UT Southwestern Medical Center researchers, maintains its biological function while resisting aggregation, a pathological trait linked to neurodegenerative diseases called tauopathies.
These findings, reported in Structure, could lead to new treatments for conditions including Alzheimer’s disease, frontotemporal dementia, chronic traumatic encephalopathy (CTE), and progressive supranuclear palsy.
“This is the first step toward creating a molecule that could, in principle, replace a protein that’s pathogenic (disease-causing) while still retaining its normal function,” said study leader Lukasz Joachimiak, Ph.D., Associate Professor in the Center for Alzheimer’s and Neurodegenerative Diseases and of Biochemistry and Biophysics at UT Southwestern.
Researchers at Lund University in Sweden have created a method that makes it possible to transform the brain’s support cells into parvalbumin-positive cells. These cells act as the brain’s rapid-braking system and are significantly involved in schizophrenia, epilepsy and other neurological conditions.
Parvalbumin cells play a central role in keeping brain activity in equilibrium. They control nerve cell signaling, reduce overactivity and make sure that the brain is working to a rhythm. Researchers sometimes describe them as the cells that “make the brain sound right.”
When these cells malfunction or decrease in number, the balance of the brain is disrupted. Previous studies suggest that damaged parvalbumin cells may contribute to disorders such as schizophrenia and epilepsy.
The amygdala consists of nuclei which can be grouped into (i) the basolateral nuclear group (BLA), (ii) the superficial cortex-like laminated region (sCLR) which contains the cortical nuclei (Co), and (iii) the centromedial nuclear group.1 The BLA consists of the lateral nucleus (LA) and basal nucleus (BA). In turn, the BA consists of the basolateral nucleus and the basomedial nucleus. The centromedial nuclear group consists of the central nucleus (Ce), medial nucleus (Me), and intercalate cell mass (IC). In turn, Ce consists of a lateral (CeL) subdivision and a medial (CeM) subdivision. The centromedial nuclear group (Ce, Me, and IC) along with the bed nucleus of the stria terminalis (BNST) and sublenticular substantia innominata together comprise the centromedial extended amygdala.
The cellular composition of the BLA nuclei and the sCLR’s Co nuclei resembles that of the cerebral cortex in that the majority of the neurons are pyramidal-like glutamatergic cells while the rest are local GABAergic inhibitory interneurons.1 The inhibitory interneurons include parvalbumin-containing neurons which mainly synapse on the soma and proximal dendrites of the pyramidal cells and somatostatin-containing neurons which mainly synapse on the distal dendrites of the pyramidal neurons. By contrast, the composition of the Ce and Me nuclei resembles the striatum in that many of the neurons are similar to GABAergic medium spiny neurons.
Viswanadham, Kim, et al. combine somatic mutational and transcriptome analyses to trace the lineages of neuronal clones in the human cerebral cortex. They explore the differences between the visual and prefrontal cortex in clonal development, dispersion, and identities and dissect the lineages of late-rising cortical glutamatergic and GABAergic neurons.