Lifeboat Foundation

Researchers have made a digital map showing a tiny chunk of a human brain in unprecedented detail.

Based on a brain tissue sample that had been surgically removed from a person, the map represents a cubic millimeter of brain—an area about half the size of a grain of rice. But even that tiny segment is overflowing with 1.4 million gigabytes of information—containing about 57,000 cells, 230 millimeters of blood vessels and 150 million synapses, the connections between neurons.

The researchers published their findings in the journal Science on Friday. They have made the data set freely available online and provided tools for analyzing and proofreading it.

Presynapses locally recycle synaptic vesicles to efficiently communicate information. During use and recycling, proteins on the surface of synaptic vesicles break down and become less efficient. In order to maintain efficient presynaptic function and accommodate protein breakdown, new proteins are regularly produced in the soma and trafficked to presynaptic locations where they replace older protein-carrying vesicles. Maintaining a balance of new proteins and older proteins is thus essential for presynaptic maintenance and plasticity. While protein production and turnover have been extensively studied, it is still unclear how older synaptic vesicles are trafficked back to the soma for recycling in order to maintain balance. In the present study, we use a combination of fluorescence microscopy, hippocampal cell cultures, and computational analyses to determine the mechanisms that mediate older synaptic vesicle trafficking back to the soma. We show that synaptic vesicles, which have recently undergone exocytosis, can differentially utilize either the microtubule or the actin cytoskeleton networks. We show that axonally trafficked vesicles traveling with higher speeds utilize the microtubule network and are less likely to be captured by presynapses, while slower vesicles utilize the actin network and are more likely to be captured by presynapses. We also show that retrograde-driven vesicles are less likely to be captured by a neighboring presynapse than anterograde-driven vesicles. We show that the loss of synaptic vesicle with bound molecular motor myosin V is the mechanism that differentiates whether vesicles will utilize the microtubule or actin networks. Finally, we present a theoretical framework of how our experimentally observed retrograde vesicle trafficking bias maintains the balance with previously observed rates of new vesicle trafficking from the soma.

Cytoskeleton-based trafficking mechanics have long been explored because of their essential role in neuronal function and maintenance (Westrum et al., 1983; Okada et al., 1995; Sorra et al., 2006; Perlson and Holzbaur, 2007; Tao-Cheng, 2007; Hirokawa et al., 2009; Staras and Branco, 2010; Tang et al., 2013; Wu et al., 2013; Maeder et al., 2014; Guedes-Dias et al., 2019; Gramlich et al., 2021; Watson et al., 2023). Protein trafficking via cytoskeleton transport is essential for synaptogenesis (Perlson and Holzbaur, 2007; Santos et al., 2009; Klassen et al., 2010; Wu et al., 2013; Guedes-Dias et al., 2019; Guedes-Dias and Holzbaur, 2019; Kurshan and Shen, 2019; Watson et al., 2023) and to replace older proteins with newer proteins for efficient function (Cohen et al., 2013; Dörrbaum et al., 2018, 2020; Heo et al., 2018; Truckenbrodt et al., 2018; Jähne et al., 2021; Watson et al., 2023).

In a discovery that could hasten treatment for patients with multiple sclerosis (MS), UC San Francisco scientists have discovered a harbinger in the blood of some people who later went on to develop the disease.

In about 1 in 10 cases of MS, the body begins producing a distinctive set of antibodies against its own proteins years before symptoms emerge. These autoantibodies appear to bind to both human cells and common pathogens, possibly explaining the immune attacks on the brain and spinal cord that are the hallmark of MS.

The findings were published in Nature Medicine on April 19.

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When Roger Penrose originally came out with the idea that the human brain uses quantum effects in microtubules and that was the origin of consciousness, many thought the idea was a little crazy. According to a new study, it turns out that Penrose was actually right… about the microtubules anyways. Let’s have a look.

Continue reading “Brain Really Uses Quantum Effects, New Study Finds” »

The brain is one of the most complex entities in biology. For thousands of years, humans have wondered how the human brain works, but only in the past few years has technology evolved so that scientists can actually answer some of the many questions we have. What are the causes of brain disorders? How do our brains develop? How does the brain heal after a head injury? While we still have a long way to go before we can understand the many facets of the human brain, one technology – CRISPR – has allowed us to start answering these questions on a genetic level.

What is CRISPR?

Imagine having telepathic conversations with loved ones, instantaneously accessing superhuman computational power, playing back memories and dreams, or immersing yourself and every sense you possess into a virtual entertainment experience. In the distant future, if brain-computer interfaces (BCIs) are successful at reading and writing information to the brain, and if humans adapt to the technology, we could experience some pretty amazing scenarios. But, there are many outstanding questions for how we could ensure a bright future: Who will own the data generated by our brains? Will brain data be bought and sold by data brokers like other personal information today? Will people be forced to use certain BCIs that surveil their brain activity (for example, to make sure you’re paying attention at work and school)? Will BCIs put peoples’ brains at risk of being hacked? As with all new technology, more of these philosophical questions will need to be investigated and answered before there is widespread adoption and use of BCIs in the future.

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Who owns that data?

Down syndrome (DS) is one of the most prevalent genetic disorders in humans. The use of new approaches in genetic engineering and nanotechnology methods in combination with natural cellular phenomenon can modify the disease in affected people. We consider two CRISPR/Cas9 systems to cut a specific region from short arm of the chromosome 21 (Chr21) and replace it with a novel designed DNA construct, containing the essential genes in chromatin remodeling for inactivating of an extra Chr21. This requires mimicking of the natural cellular pattern for inactivation of the extra X chromosome in females. By means of controlled dosage of an appropriate Nano-carrier (a surface engineered Poly D, L-lactide-co-glycolide (PLGA) for integrating the relevant construct in Trisomy21 brain cell culture media and then in DS mouse model, we would be able to evaluate the modification and the reduction of the active extra Chr21 and in turn reduce substantial adverse effects of the disease, like intellectual disabilities. The hypothesis and study seek new insights in Down syndrome modification.

Keywords: Down syndrome, CRISPR/Cas9, Designed DNA construct, Poly D L-lactide-co-glycolide (PLGA), Nano-carrier, Chromosome 21 inactivation.

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This spring, the Hastings Center Report added a new series of essays named after the field its pieces aim to explore. Neuroscience and Society produces open access articles and opinion pieces that address the ethical, legal, and societal issues presented by emerging neuroscience. The series will run roughly twice a year and was funded by the Dana Foundation to foster dynamic, sustained conversation among neuroscience researchers, legal and ethics scholars, policymakers, and wider publics.

The first edition of the series focuses on the topic of research studies and what is owed to people who volunteer to participate in clinical trials to develop implantable brain devices, such as deep-brain stimulators and brain-computer interfaces.

Imagine you have lived with depression for most of your life. Despite trying numerous medications and therapies, such as electroconvulsive therapy, you have not been able to manage your symptoms effectively. Your depression keeps you from maintaining a job, interacting with your friends and family, and generally prevents you from flourishing as a person.

Here is an interview concerning the current AI and generative AI waves, and their relation to neuroscience. We propose solutions based on new technology from neuroAI – which includes humans ability for reasoning, thought, logic, mathematics, proof etc. – and are therefore poorly modeled by data analysis on its own. Some of our work – also with scholars – has been published, while more is to come in a spin-off setting.