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The article discusses the impact of A{beta} amyloidosis on axonal pathology in Alzheimer's disease. Through various imaging methods, researchers observed widespread axonal amyloidosis with distinctive enlargement in AD brains. This enlargement was associated with lysosome destabilization, chronic microhemorrhage, and other markers of neuronal damage, highlighting a major defect in Alzheimer's disease. The study suggests a link between amyloidosis, lysosome destabilization, and axonal pathology in AD, shedding light on potential mechanisms underlying the disease. [Extracted from the article]

A recent study from Newcastle University explores the role of cell surface extensions in connecting sensory processing across the dorsal horn of the mouse spinal cord. The research focuses on spinal projection neurons and their axon collaterals, shedding light on their function in local spinal sensory processing and relaying sensory signals to the brain. Financial support for this study was provided by various organizations including the National Health And Medical Research Council and the Biotechnology And Biological Sciences Research Council. For more information, the full article can be accessed for free at the publisher's website. [Extracted from the article]

Researchers at the University of California Irvine have found that dendrite injury triggers neuroprotection in Drosophila models of neurodegenerative diseases. By inducing injury to a single primary dendrite branch, they were able to protect against dendrite loss in neurons modeling polyglutamine diseases. This study suggests that activating dendrite regeneration pathways could potentially slow or reverse dendrite loss in neurodegenerative diseases. The findings were published in Scientific Reports and can be accessed for free online. [Extracted from the article]

A recent study conducted at the University of Padua in Italy explored the effects of Alpine viper venom on the central nervous system. The research found that a small molecule agonist of the CXCR4 receptor, called NUCC-390, showed promise in rapidly recovering motor axon terminals affected by the venom, leading to functional restoration of the neuromuscular junction. This discovery suggests NUCC-390 could be a potential therapeutic option for individuals suffering from paralysis due to snakebites. The study was supported by the Italian Ministry of Defence, the Slovenian Research Agency, and the Universita degli Studi di Padova. [Extracted from the article]

The article explores the synaptic targets and cellular sources of CB1 cannabinoid receptor and vesicular glutamate transporter-3 expressing nerve terminals in relation to GABAergic neurons in the human cerebral cortex. It discusses the regulation of synaptic transmission by CB1 receptors in nerve terminals and the co-transmission of GABA and glutamate from single cortical interneurons. The study reveals the presence of multiple vesicular glutamate transporters in a select population of terminals in the human cerebral cortex. [Extracted from the article]

Cornell University has been issued a patent for methods of expressing proteins in axons, which are long extensions of neurons that connect to target cells. The patent aims to promote axonal regeneration or growth after injury by transducing protein-coding sequences into mammalian axons using RNA viruses. The invention provides isolated recombinant nucleic acids and RNA viruses that can deliver polypeptide-coding sequences into axons for expression, offering potential treatments for conditions associated with aberrant axon function. [Extracted from the article]

A team of Canadian and American scientists, led by researchers from the University of Montreal and the University of Pennsylvania, has made a breakthrough in understanding mirror movement disorder, a neurological disorder characterized by involuntary movements in the arms and hands. Mirror movement disorder can cause pain and difficulties in performing tasks requiring left-right coordination. The researchers discovered that the cellular mechanism behind mirror movements is a defect in axon guidance, a process that controls the elongation and navigation of neurons' axons. This finding could lead to new targets for treatment and provide insights into other nervous system disorders. [Extracted from the article]

Ge Precision Healthcare LLC has been issued a patent for neuromodulation techniques. The patent describes methods for modulating a physiological response using energy applied from an energy source. Neuromodulation has been used to treat various clinical conditions, such as chronic back pain and movement disorders. The patent focuses on non-invasive and non-thermal techniques, such as applying ultrasound energy to nerve plexuses or ganglions, to induce a non-thermal, mechanical stimulation of sensory nerve pathways. These techniques aim to reduce insulin resistance and modulate metabolic function. The patent also discusses the challenges of positioning electrodes near target nerves and the potential for more selective and targeted neuromodulation effects. [Extracted from the article]

A recent report from Beijing University of Chinese Medicine discusses the role of primary cilia (PC) in Parkinson's disease (PD). PC are sensory organelles found in various types of cells, including astrocytes and neurons, and they send signals to control physiological and cellular processes by detecting changes in the extracellular environment. In PD, abnormalities in the structure and function of PC contribute to the progression of the disease by influencing signaling pathways, genes, defective mitochondrial function, and dopaminergic neurons in the substantia nigra. The review aims to provide references and ideas for future research on the function and pathological mechanisms of PC in neurodegenerative diseases like PD. [Extracted from the article]

Researchers at Stanford University have developed a new method to help bring misplaced proteins back to their proper locations within cells. Misplaced proteins are associated with diseases such as cancer and neurodegenerative disorders. The method involves using naturally occurring shuttles within cells to transport the proteins to their correct destinations. The researchers have created a new class of molecules called "targeted relocalization activating molecules" (TRAMs) that convince the shuttles to carry the proteins to different parts of the cell. This strategy could potentially lead to therapeutics for correcting protein misplacement and creating new functions in cells. [Extracted from the article]

A preprint abstract from biorxiv.org discusses the role of mitophagy in neurodegenerative diseases such as Parkinson's disease. The study found that damaged axonal mitochondria are targeted for degradation through mitophagy at presynapses, which are the primary sites for this process. When mitophagy is defective, presynapses become vulnerable, leading to neurodegeneration. The researchers also discovered that synthetic upregulation of receptor-mediated mitophagy using the compound Roxadustat could potentially be a therapeutic approach for these diseases. However, it is important to note that this preprint has not yet undergone peer review. [Extracted from the article]

A report from Yale University discusses new research findings on spinal cord injury and its impact on spasticity, a hyperexcitability disorder that affects functional recovery. The study focuses on the role of astrocytes, a type of cell in the central nervous system, in post-injury hyperreflexia and plasticity of neighboring neuronal synaptic dendritic spines. The researchers found that selective Rac1KO in astrocytes reduced hyperreflexia and dendritic spine dysgenesis, potentially enhancing glutamate clearance and reducing spasticity. These findings suggest that targeting cell-specific molecular regulators could be a potential strategy for managing spasticity after spinal cord injury. [Extracted from the article]

A recent study conducted by researchers at the Medical University of Silesia highlights the role of primary cilia in retinal degeneration. Primary cilia are sensory organelles found in various cell types and play a crucial role in detecting and transmitting signaling pathways. The dysfunction of primary cilia can lead to a range of clinical manifestations known as ciliopathies, with retinal degeneration being a common occurrence. The study explores the occurrence of primary cilia in different retinal cell types and their significance in pathology, as well as potential therapeutic approaches for ciliopathies. This research provides new insights and innovative concepts for the investigation and treatment of retinal degenerative diseases. [Extracted from the article]

A recent report from Osaka University in Japan discusses the importance of Rab6, a small GTPase, in the regulation of intracellular vesicular trafficking and neuronal polarization. The researchers found that Rab6-mediated polarized transport of synaptic vesicle precursors (SVPs) is crucial for the establishment of neuronal polarity and brain formation. In their study, they observed that mice with a double knockout of Rab6a/b exhibited severe dysplasia of the neocortex and cerebellum, as well as impaired axonal extension and loss of axon-dendrite polarity. These findings contribute to our understanding of the mechanisms involved in neuronal development and brain function. [Extracted from the article]

A recent study conducted at the University of Wisconsin Madison explored the potential therapeutic effects of increasing nicotinamide adenine dinucleotide (NAD+) availability in amyotrophic lateral sclerosis (ALS). The researchers found that supplementation with the NAD+ precursor nicotinamide mononucleotide (NMN) increased the complexity of neuronal processes and prevented neuronal death in motor neurons isolated from ALS mouse models and induced pluripotent stem cell-derived human motor neurons. Additionally, NMN treatment normalized the cytoplasmic mislocalization of transactive response DNA binding protein-43 (TDP-43) induced by its overexpression. These findings suggest that NAD+ precursor supplementation may have therapeutic potential in both sporadic and familial ALS. [Extracted from the article]

A preprint abstract from biorxiv.org discusses the associative plasticity of granule cell inputs to cerebellar Purkinje cells. The study explores the possibility that the ascending axon (AA) and parallel fiber (PF) synapses encode different information and trigger plasticity when associated with each other. The researchers found that synchronous AA and PF repetitive train stimulation can induce long-term potentiation (LTP) specifically at AA synapses. The timing of the two inputs also affects the outcome of plasticity, and the activation of NMDAR and mGluR1 is required for induction. This research suggests that AA and PF synapses have different coding capabilities and associative plasticity, allowing for effective association of information transmitted via granule cells. [Extracted from the article]

A new report discusses research conducted at Hainan Medical University in Haikou, People's Republic of China, on the effects of Calycosin (CA) on spinal cord injury (SCI). The study aimed to explore the influence of CA on SCI by promoting axon growth. The researchers found that CA treatment increased neuronal process outgrowth and the expressions of axon regeneration markers in both SCI model rats and primary cortical neurons. They concluded that CA improves SCI by increasing axon development through regulating the expression of the protein tyrosine phosphatase receptor type S (PTPRS). [Extracted from the article]

A study conducted by the Institute of Molecular Life Sciences in Budapest, Hungary, explored the effects of typical and atypical antipsychotic agents on human neural progenitor cells. The researchers found that antipsychotic medications did not affect the growth properties of the cells but did significantly alter neurite outgrowth, which is the extension of cell surfaces. The study also observed subtle changes in gene expression levels related to neuronal identity. Overall, the findings suggest that antipsychotics promote neurogenesis by influencing neurite outgrowth rather than cell survival or gene expression. This research provides insights into the effects of antipsychotics on neuronal differentiation and highlights the importance of considering neurite outgrowth as a potential target of action. [Extracted from the article]

A recent study conducted at the University of Iowa explored the role of the Pcdhg gene cluster in neural development. The researchers used CRISPR/Cas9 genome editing to create two mouse lines that expressed non-phosphorylatable gamma-Pcdhs, resulting in increased dendrite arborization in cortical pyramidal neurons. The study confirmed that phosphorylation of a shared C-terminal motif is a key negative regulation point for gamma-Pcdh and shed light on the distinct roles played by individual isoforms and protein domains. This research provides valuable insights into the mechanisms underlying dendrite arborization in the cerebral cortex. [Extracted from the article]

A preprint abstract from biorxiv.org discusses the relationship between amyloidosis and axon pathology in Alzheimer's disease (AD). The study used histochemistry, immunohistochemistry, and fluorescence imaging to examine axonal phenotypes in AD brains. The researchers found that axonal amyloidosis was widespread in AD brain tissues and was associated with axonal enlargement, loss of axonal structural protein MAP2, Tau phosphorylation, lysosome destabilization, and markers of hemorrhagic insults. The study suggests that axonal amyloidosis and enlargement, along with chronic microhemorrhage and lysosome destabilization, are major neurological defects in AD. However, it is important to note that this preprint has not been peer-reviewed. [Extracted from the article]

Researchers from Brown University have discovered that a majority of parvalbumin-expressing (PV+) interneurons in the upper layers of the mouse neocortex exhibit ectopic action potentials (EAPs) after sufficient activation of their somata. EAPs are action potentials that initiate at sites distal to the axon initial segment and propagate antidromically along the axon. This finding suggests that ectopic spiking of PV+ interneurons is common and may contribute to both normal and pathological network functions of the neocortex. The research was supported by the National Institute of Neurological Disorders and Stroke. [Extracted from the article]

This article discusses a study on the role of primary cilia in postnatal neurodevelopment. The researchers found that primary cilia in principal neurons undergo changes in positioning and orientation during postnatal development in the mouse cerebral cortex. They also discovered that the cell bodies of principal neurons in certain brain regions undergo a slow reverse movement for postnatal positioning and lamina refinement. Disruption of cilia function in the forebrain led to altered cortical lamination. This research suggests that primary cilia play a role in neuronal positioning and the refinement of the cerebral cortex. [Extracted from the article]

A recent report from the University of Toronto provides new insights into central nervous system disorders, specifically experimental autoimmune encephalomyelitis (EAE), which is a common immune-based model of multiple sclerosis (MS). The severity of EAE is typically measured using a clinical scale, but this scale may not accurately assess recovery from the disease. The report presents a simple protocol for scoring inflammation, demyelination, and axonal injury in the spinal cord and brain sections of mice, as well as a method for measuring overall central nervous system injury in live mice. The research aims to better understand the underlying mechanisms of cellular injury in the central nervous system. [Extracted from the article]

According to a preprint abstract from biorxiv.org, researchers have found that the protein Numb plays a central role in the repulsion of axons in the central nervous system. The study focused on two specific processes: the repulsion of retinal ganglion cell axons at the optic chiasm and the repulsion of commissural axons in the spinal cord. The researchers discovered that Numb is essential for both of these repulsion processes, positioning it as a key player in the non-canonical Sonic hedgehog signaling pathway. It is important to note that this preprint has not yet undergone peer review. [Extracted from the article]

A recent preprint abstract discusses the discovery of synaptic nanostructures and their role in the flexibility of synaptic function in the brain. The study used advanced imaging techniques to analyze the organization of glutamatergic synapses in the neocortex. The researchers found that different types of synapses exhibited diverse nano-organization patterns, depending on the afferent input and sub-cellular localization. This research provides valuable insights into the complex organization of synapses in the brain. However, it is important to note that this preprint has not yet undergone peer review. [Extracted from the article]

A recent study conducted by researchers at the University of Cologne's CECAD Cluster of Excellence in Aging Research has shed light on the process of neuronal maturation and plasticity in the brain. The study focused on the role of mitochondrial fusion in the development of new neurons in the hippocampus, a region associated with cognition and emotional behavior. The researchers found that mitochondrial fusion plays a crucial role in sustaining the plasticity of new synapses and refining pre-existing brain circuits. These findings have implications for understanding neurological disorders and may guide future interventions to restore cognitive function. [Extracted from the article]

A preprint abstract from biorxiv.org discusses the role of the KMN network, which is primarily known for its involvement in chromosome segregation, in neurodevelopment. The study focuses on the C. elegans head nervous system and demonstrates that the KMN network is crucial for establishing proper axonal organization. Specifically, the degradation of the KNL-1 protein leads to disorganized ganglia and abnormal axon placement and organization. The study also highlights the importance of signaling motifs within KNL-1 for recruiting protein phosphatase 1 and activating the spindle assembly checkpoint during neurodevelopment. Additionally, the NDC-80 microtubule-binding mutant is found to play a role in facilitating axon-axon contacts. These findings suggest a non-canonical role for the KMN network in shaping the structure and connectivity of the nervous system during brain development in C. elegans. However, it is important to note that this preprint has not yet undergone peer review. [Extracted from the article]

Researchers at the University of California have presented data on spinal cord injury, focusing on the use of multichannel bridges and human neural stem cells (hNSC) to enhance axon regeneration, myelination, synaptic reconnection, and recovery. The study found that acute implantation of a multichannel bridge mechanically stabilizes the injury and promotes axonal regrowth. Additionally, the transplantation of hNSC on a poly(lactide-co-glycolide) (PLG) scaffold increased the myelination of axons. The combination of acute bridge implantation and hNSC transplantation showed promising results in improving locomotor recovery. [Extracted from the article]

A research group led by Kazunobu Sawamoto at Nagoya City University and the National Institute for Physiological Sciences has discovered that the growth cone in migrating neurons plays a crucial role in promoting neuronal migration and regeneration in the brain after injury. The researchers used super-resolution microscopy to study the structure and function of the growth cone and found that it responds to external signals through tyrosine phosphatase receptor type sigma (PTPs) to guide the directionality of migration. They also found that the growth cone can revert to its extended morphology and enable neuronal migration when it interacts with heparan sulfate (HS). The researchers applied HS-containing biomaterial to the injured brain and observed that it promoted the extension of growth cones, neuronal migration, and the regeneration of mature neurons. These findings suggest that understanding the molecular mechanisms of growth cone-mediated interaction with the extracellular environment could lead to the development of new regeneration technologies for promoting neuronal migration. [Extracted from the article]

A research study conducted at the Sixth Affiliated Hospital of Xinjiang Medical University in Urumqi, China, analyzed the therapeutic effects of microRNAs on axonal regeneration after peripheral nerve injury. The study used bibliometric methods to identify research hotspots and future development trends in this field. A total of 174 articles met the research criteria and were authored by individuals from 24 countries and 199 institutions. The study concluded that microRNAs have become a hot topic in neural inflammation, cell repair and regeneration, protection, and functional recovery, and further research in this area could lead to advancements in the treatment of peripheral nerve injury. [Extracted from the article]

The US Patent and Trademark Office has published a patent application titled "Compositions For and Methods of Enhancing Spinal Cord Tissue Regeneration" by inventors from Duke University. The application aims to address the need for enhancing spinal cord tissue regeneration in adult mammals. The inventors propose the use of compositions containing HB-EGF and isolated nucleic acid molecules to promote axon regeneration and functional recovery in spinal cord injuries. The application also includes information on plasmids, transgene cassettes, transgenic animals, and vectors that can be used in the proposed methods. The patent application provides detailed information on specific nucleic acid sequences, vectors, and methods used for treating spinal cord injuries. [Extracted from the article]

According to a preprint abstract, researchers have discovered that a protein called NEKL-4 plays a role in regulating the stability of cilia, which are cell surface extensions involved in various cellular functions. The study was conducted using the model organism C. elegans and found that NEKL-4 is associated with mitochondria and influences ciliary stability by activating certain proteins and promoting mitochondrial homeostasis. This research has not yet undergone peer review. [Extracted from the article]

A recent study conducted by the Polish Academy of Sciences examined the role of astrocytes in guiding the axon pathways of newly generated neocortical neurons in the opossum Monodelphis domestica. The researchers found that upper-layer neurons in the opossum expressed proteins known to be essential for the formation of the corpus callosum in other mammals, suggesting that extrinsic cues play a significant role in guiding axons in the opossum. Additionally, the study identified a small population of astrocytes in the midline area of the anterior commissure, which may help guide neocortical axons to cross the midline. This research provides valuable insights into the development of the neocortex in marsupials and contributes to our understanding of axon guidance pathways in different species. [Extracted from the article]

A study conducted by researchers from King's College London explores the impact of functional changes to the axon initial segment (AIS) on neuronal excitability in amyotrophic lateral sclerosis (ALS) human induced pluripotent stem cell (hiPSC) motor neurons. The study found that early ALS hiPSC motor neurons exhibited an increase in AIS length and impaired activity-dependent AIS plasticity, leading to abnormal regulation of neuronal activity and intrinsic hyperexcitability. In contrast, late ALS hiPSC and postmortem ALS motor neurons showed AIS shortening and hypoexcitability. The study suggests that the AIS is a significant site of dysfunction in ALS motor neurons. [Extracted from the article]

A recent study conducted at Cedars Sinai Medical Center in Los Angeles, California, has identified a specific subtype of human nucleus pulposus cells (NPCs) associated with the onset of discogenic back pain. The researchers used single-cell transcriptomic analysis to establish a strong correlation between this cell subtype and the pain condition associated with degenerated discs. In vitro experiments demonstrated that these stimulated NPCs triggered pain-associated responses in sensory neurons. Injection of stimulated NPCs into healthy rat intervertebral discs induced local inflammatory responses and increased sensitivity to cold and mechanical stimuli. These findings could potentially contribute to the development of targeted therapeutic strategies for discogenic low back pain. [Extracted from the article]

A recent report from the University of North Carolina discusses the mapping of neuronal and glial primary cilia contactome and connectome in the human cerebral cortex. Primary cilia act as antenna receivers of environmental signals and disruptions in their function can lead to circuit disorders. The researchers comprehensively mapped the contacts of cilia within the human cortical connectome and found that primary cilia display variations in size, shape, and microtubule axoneme core, which may affect their signaling competencies. This diversity in the structure, contactome, and connectome of primary cilia gives each neuron or glial cell a unique barcode of access to the surrounding neural circuitry. [Extracted from the article]

According to a preprint abstract, activating LRRK2 mutations cause Parkinson's disease. The loss of primary cilia in specific striatal cell types, such as cholinergic interneurons and astrocytes, is associated with decreased neuroprotection for dopamine neurons in both mice and humans with Parkinson's disease. Medium spiny neurons, on the other hand, maintain normal cilia and have higher LRRK2 expression. These findings suggest that the loss of cilia in certain striatal cell types may contribute to the development and progression of Parkinson's disease. However, it is important to note that this research has not yet undergone peer review. [Extracted from the article]

A recent report from the Center for Research explores the role of caffeine in neuroprotection for Parkinson's Disease (PD). The study investigates the effects of caffeine on anti-apoptotic function, neurite growth, calcium homeostasis, and autophagy. The research found that caffeine demonstrated neuroprotective effects and reduced apoptotic cell death in neuronal cells. Additionally, caffeine was shown to maintain neurite length, restore calcium levels, and induce autophagy. This study suggests that caffeine may have potential therapeutic benefits for individuals with Parkinson's Disease. [Extracted from the article]

According to a preprint abstract, researchers have discovered a pathway in which cilia, the hair-like structures on brain neurons, are deconstructed during the development of cerebellar granule cells. Through single cell transcriptomic and immunocytological analyses, the researchers found that the transcription of genes required for cilia maintenance decreased during differentiation, leading to cilia loss. Additionally, the binding of centriolar cap proteins to the mother centrioles prevented cilia regrowth. These findings suggest a developmentally programmed mechanism for cilia deconstruction in differentiating granule cells. However, it is important to note that this preprint has not yet undergone peer review. [Extracted from the article]

A recent preprint abstract discusses the role of a protein called CLUH in maintaining the health and function of axons in spinal motoneurons. The study found that CLUH is essential for preventing axonal degeneration and maintaining motor behavior in mice. CLUH binds to mRNAs encoding mitochondrial proteins and helps protect mitochondria from damage during their journey along the axon. The absence of CLUH leads to deficits in ATP production specifically in the growth cone of axons. The study highlights the importance of CLUH in mitochondrial quality control and translational regulation in axons for their development and long-term integrity. [Extracted from the article]

A preprint abstract from biorxiv.org discusses the associative plasticity of granule cell inputs to cerebellar Purkinje cells. The study suggests that the synapses formed by the ascending axon (AA) and parallel fiber (PF) segments of the granule cell axon may encode different information. The researchers found that synchronous stimulation of AA and PF inputs triggers long-term potentiation (LTP) specifically at AA synapses. The timing of the two inputs and the activation of certain receptors also play a role in plasticity. This research provides insights into the coding capabilities and plasticity of AA and PF synapses, enabling effective association of information transmitted via granule cells. [Extracted from the article]

Researchers from Yonsei University in Seoul, South Korea have developed a multi-channel collagen conduit with aligned Schwann cells and endothelial cells to enhance neuronal regeneration in spinal cord injury (SCI). The conduit was fabricated using extrusion 3D bioprinting and showed promising results in promoting axon elongation, proliferation, remyelination, inflammation reduction, and angiogenesis in vitro and in vivo. The study highlights the importance of understanding the biological environment during regeneration to overcome the disruption of vasculature and ischemia caused by SCI. This research provides a new therapeutic strategy for SCI and has been peer-reviewed. [Extracted from the article]