Donald Hoffman and Hannah Critchlow debate the origins of consciousness.
This excerpt was taken from “The key to consciousness,” featuring Sam Coleman, Donald Hoffman, and Hannah Critchlow. Joanna Kavenna hosts.
One day in the future, we may interact with our electronic devices not with physical input or even voice commands, but simply by thinking about what we want to do. Such brain–computer interfaces (BCIs), combined with machine learning, could allow us to turn our ideas into reality faster and with less effort than ever before — imagine being able to produce a PCB design simply by thinking about how the completed circuit would work. Of course as an assistive technology, BCIs would be nothing less than life-changing for many.
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In the adult brain, synapses are tightly enwrapped by lattices of the extracellular matrix that consist of extremely long-lived molecules. These lattices are deemed to stabilize synapses, restrict the reorganization of their transmission machinery, and prevent them from undergoing structural or morphological changes. At the same time, they are expected to retain some degree of flexibility to permit occasional events of synaptic plasticity. The recent understanding that structural changes to synapses are significantly more frequent than previously assumed (occurring even on a timescale of minutes) has called for a mechanism that allows continual and energy-efficient remodeling of the extracellular matrix (ECM) at synapses. Here, we review recent evidence for such a process based on the constitutive recycling of synaptic ECM molecules. We discuss the key characteristics of this mechanism, focusing on its roles in mediating synaptic transmission and plasticity, and speculate on additional potential functions in neuronal signaling.
An increasing number of studies are showing that synaptic function is strongly influenced by their local environment, including the molecules or cellular components in their vicinity. As a result, the classical synaptic framework (consisting of the pre-and postsynaptic compartments only) has gradually been extended to include the neighboring astrocytic processes (the “tripartite synapse”; Araque et al., 1999) and, ultimately, also the surrounding extracellular matrix (ECM; the “tetrapartite synapse”; Dityatev et al., 2006). Nowadays, the synaptic ECM is recognized to play an essential role in physiological synaptic transmission as well as in plasticity, and its dysregulation has been linked to synaptopathies in a wide variety of brain disorders (Bonneh-Barkay and Wiley, 2009; Pantazopoulos and Berretta, 2016; Ferrer-Ferrer and Dityatev, 2018).
We often imagine that human consciousness is as simple as input and output of electrical signals within a network of processing units — therefore comparable to a computer. Reality, however, is much more complicated. For starters, we don’t actually know how much information the human brain can hold.
The pursuit of a cure for Alzheimer’s disease is becoming an increasingly competitive and contentious quest with recent years witnessing several important controversies.
In July 2022, Science magazine reported that a key 2006 research paper, published in the prestigious journal Nature, which identified a subtype of brain protein called beta-amyloid as the cause of Alzheimer’s, may have been based on fabricated data.
One year earlier, in June 2021, the US Food and Drug Administration had approved aducanumab, an antibody-targeting beta-amyloid, as a treatment for Alzheimer’s, even though the data supporting its use were incomplete and contradictory.
Researchers at Boston University, U.S. report that the flow of cerebrospinal fluid in the brain is linked to waking brain activity. Led by Stephanie Williams, and publishing in the open access journal PLOS Biology on March 30, the study demonstrates that manipulating blood flow in the brain with visual stimulation induces complementary fluid flow. The findings could impact treatment for conditions like Alzheimer’s disease, which have been associated with declines in cerebrospinal fluid flow.
Just as our kidneys help remove toxic waste from our bodies, cerebrospinal fluid helps remove toxins from the brain, particularly while we sleep. Reduced flow of cerebrospinal fluid is known to be related to declines in brain health, such as occur in Alzheimer’s disease. Based on evidence from sleep studies, the researchers hypothesized that brain activity while awake could also affect the flow of cerebrospinal fluid. They tested this hypothesis by simultaneously recording human brain activity via fMRI and the speed of cerebrospinal fluid flow while people were shown a checkered pattern that turned on and off.
Researchers first confirmed that the checkered pattern induced brain activity; blood oxygenation recorded by fMRI increased when the pattern was visible and decreased when it was turned off. Next, they found that the flow of cerebrospinal fluid negatively mirrored the blood signal, increasing when the checkered pattern was off. Further tests showed that changing how long the pattern was visible affected blood and fluid in a predictable way, and that the blood-cerebrospinal fluid link could not be accounted for by only breathing or heart rate rhythms.
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My name is Artem, I’m a computational neuroscience student and researcher. In this video we talk about cognitive maps – internal models of outside world that the brain to generate flexible behavior that is generalized across contexts.
The hNSCs used in the study have been produced and characterised in the Cell Factory and Biobank of Santa Maria Hospital (Terni, Italy), authorised by the Italian Medicine Agency (AIFA) for the production of hNSCs to be used for clinical trials (aM 54/2018). The methodology applied to isolate, expand, characterise and cryopreserve the lines is based on the Neurosphere Assay26,41,54, and has been used for the production of the cells utilised in phase I trials for Amyotrophic Lateral Sclerosis patients (NCT0164006723) and for Secondary Progressive Multiple Sclerosis patients (NCT03282760, ongoing).
The entire production process, starting from tissue procurement to cryopreservation is compliant to cGMP guidelines and approved by AIFA. The hNSCs are obtained from foetal brain tissue derived from fetuses that underwent miscarriage or natural in utero death upon receiving the signed informed consent from the mother. Forty-eight hours prior to implantation, hNSCs were plated in the growth medium at a concentration of 10,000 cells/cm2. On the day of surgery, hNSCs were collected by centrifugation, viable cells were counted by Trypan blue exclusion criteria, and the correct number of cells were re-suspended in HBSS for the transplant.
SOD1 transgenic male rats were randomly divided into three experimental groups: (i) transplanted with hNSCs (hNSC rats, n = 15); (ii) treated with HBSS (HBSS rats, n = 15) and (iii) untreated (CTRL rats, n = 22). An additional group of non-transgenic littermates (wild-type, WT, n = 9) were used as controls for symptomatic evaluation of the colony. Tacrolimus (FK506) and cyclosporine (cyclosporin A) are the principal immunosuppressive drugs that have been applied for solid organ transplantation55,56 and have been translated to stem cell treatments for PD57 and ALS22. In animal models, despite differences in potency, both drugs showed excellent survival rates for grafts across many comparative studies58,59. Our previous results44,45 showed that hNSCs can survive—without signs of rejection—in the rat brain up to 6 months under transient immunosuppression treatment, with cyclosporin A. On the bases of these results, we applied the same immunosuppressive treatment with administration of cyclosporine A (15 mg/kg/day subcutaneous; Sandimmne, Novartis) that was initiated on the day of transplantation and continued for 15 days after surgery (for all animal groups).
Alzheimer’s disease is a very common illness that affects older people worldwide, and it is one of the main causes of dementia. Researchers have been working for more than twenty years to find out what causes Alzheimer’s, but they have not yet discovered the exact reason, and there is no cure for the disease.
Huntington’s disease (HD) is a neurodegenerative disease caused by a CAG repeat expansion in the Huntingtin (HTT) gene. The resulting polyglutamine (polyQ) tract alters the function of the HTT protein. Although HTT is expressed in different tissues, the medium spiny projection neurons (MSNs) in the striatum are particularly vulnerable in HD. Thus, we sought to define the proteome of human HD patient–derived MSNs. We differentiated HD72 induced pluripotent stem cells and isogenic controls into MSNs and carried out quantitative proteomic analysis. Using data-dependent acquisitions with FAIMS for label-free quantification on the Orbitrap Lumos mass spectrometer, we identified 6,323 proteins with at least two unique peptides. Of these, 901 proteins were altered significantly more in the HD72-MSNs than in isogenic controls. Functional enrichment analysis of upregulated proteins demonstrated extracellular matrix and DNA signaling (DNA replication pathway, double-strand break repair, G1/S transition) with the highest significance. Conversely, processes associated with the downregulated proteins included neurogenesis-axogenesis, the brain-derived neurotrophic factor-signaling pathway, Ephrin-A: EphA pathway, regulation of synaptic plasticity, triglyceride homeostasis cholesterol, plasmid lipoprotein particle immune response, interferon-γ signaling, immune system major histocompatibility complex, lipid metabolism and cellular response to stimulus. Moreover, proteins involved in the formation and maintenance of axons, dendrites, and synapses (e.g., Septin protein members) were dysregulated in HD72-MSNs. Importantly, lipid metabolism pathways were altered, and using quantitative image, we found analysis that lipid droplets accumulated in the HD72-MSN, suggesting a deficit in the turnover of lipids possibly through lipophagy. Our proteomics analysis of HD72-MSNs identified relevant pathways that are altered in MSNs and confirm current and new therapeutic targets for HD.
