It is hypothesized that the topology of brain networks is constructed by connecting nodes which may be continuously remodeled by appropriate training. Efficiency of physical and/or mental training on the brain relies on the flexibility of networks' architecture molded by local remodeling of proteins and synapses of excitatory neurons producing transformations in network topology. Continuous remodeling of proteins of excitatory neurons is fine-tuning the scaling and strength of excitatory synapses up or down via regulation of intra-cellular metabolic and regulatory networks of the genome-transcriptome-proteome interface. Alzheimer's disease is a model of "energy cost-driven small-world network disorder" with dysfunction of high-energy cost wiring as the network global efficiency is impaired by the deposition of an informed agent, the amyloid-β, selectively targeting high-degree nodes. In schizophrenia, the interconnectivity and density of rich-club networks are significantly reduced. Training-induced homeostatic synaptogenesis-enhancement, presumably via reconfiguration of brain networks into greater small-worldness, appears essential in learning, memory, and executive functions. A macroscopic cartography of creation-removal of synaptic connections in a macro-network, and at the intra-cellular scale, micro-networks regulate the physiological mechanisms for the preferential attachment of synapses. The strongest molecular relationship of exercise and functional connectivity was identified for brain-derived neurotrophic factor (BDNF). The allele variant, rs7294919, also shows a powerful relationship with the hippocampal volume. How the brain achieves this unique quest of reconfiguration remains a puzzle. What are the underlying mechanisms of synaptogenesis promoting communications brain ↔ muscle and brain ↔ brain in such trainings? What is the respective role of independent mental, physical, or combined-mental-physical trainings? Physical practice seems to be playing an instrumental role in the cognitive enhancement (brain ↔ muscle com.). However, mental training, meditation or virtual reality (films, games) require only minimal motor activity and cardio-respiratory stimulation. Therefore, other potential paths (brain ↔ brain com.) molding brain networks are nonetheless essential. Patients with motor neuron disease/injury (e.g., amyotrophic lateral sclerosis, traumatism) also achieve successful cognitive enhancement albeit they may only elicit mental practice.
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http://dx.doi.org/10.3389/fnagi.2015.00117 | DOI Listing |
Eur J Nucl Med Mol Imaging
January 2025
Division of Oncology, Department of Medicine I, Medical University of Vienna, Vienna, Austria.
This joint practice guideline/procedure standard was collaboratively developed by the European Association of Nuclear Medicine (EANM), the Society of Nuclear Medicine and Molecular Imaging (SNMMI), the European Association of Neuro-Oncology (EANO), and the PET task force of the Response Assessment in Neurooncology Working Group (PET/RANO). Brain metastases are the most common malignant central nervous system (CNS) tumors. PET imaging with radiolabeled amino acids and to lesser extent [F]FDG has gained considerable importance in the assessment of brain metastases, especially for the differential diagnosis between recurrent metastases and treatment-related changes which remains a limitation using conventional MRI.
View Article and Find Full Text PDFNat Commun
January 2025
State Key Laboratory of Membrane Biology, Beijing Frontier Research Center of Biological Structure, Beijing Advanced Innovation Center for Structural Biology, School of Life Sciences, Tsinghua University, Beijing, China.
SNARE (soluble N-ethylmaleimide sensitive factor attachment protein receptor) proteins are the minimal machinery required for vesicle fusion in eukaryotes. Formation of a highly stable four-helix bundle consisting of SNARE motif of these proteins, drives vesicle/membrane fusion involved in several physiological processes such as neurotransmission. Recycling/disassembly of the protein machinery involved in membrane fusion is essential and is facilitated by an AAA+ ATPase, N-ethylmaleimide sensitive factor (NSF) in the presence of an adapter protein, α-SNAP.
View Article and Find Full Text PDFNeurology
December 2024
From the Multimodal Neuroimaging Group, Department of Nuclear Medicine (G.N.B., E.J., K.G., A.D.), Department of Psychiatry (F.J.), Department of Neurology (O.A.O., E.K., P.H.W.), Medical Faculty and University Hospital of Cologne, University of Cologne; Molecular Organization of the Brain (G.N.B., A.D.), Institute for Neuroscience and Medicine II, Research Center Juelich; German Center for Neurodegenerative Diseases (F.J.), Bonn/Cologne, Germany; Institute for Translational Research (S.O.B.), and Department of Family Medicine (S.O.B.), Texas College of Osteopathic Medicine, University of North Texas Health Science Center, Fort Worth; and Cognitive Neuroscience (P.H.W.), Institute for Neuroscience and Medicine (INM-3), Research Center Juelich, Germany.
Eur J Endocrinol
November 2024
Service de Biochimie et biologie moléculaire, Hospices Civils de Lyon, Bron 69500, France.
Objective: The aim of this study was to evaluate the performance of different biomarkers for the detection of carcinoid heart disease (CHD) in neuroendocrine tumours (NETs), in particular serum 5-HIAA (s5HIAA).
Design: An explorative ancillary study of the French CrusoeNET cohort.
Methods: Patients managed in the Lyon-EURACAN Center of Excellence (CoE) were included when they were aged of at least 18 years, treated and followed for an advanced/metastatic ileum or lung NET, a NET irrespective of the primary location or from unknown primary location but with clinical CS, and/or elevation of urinary 5-HIAA (u5HIAA) twice greater than the upper limit of normal.
Introduction: With the advent of disease-modifying therapies, accurate assessment of biomarkers indicating the presence of disease-associated amyloid beta (Aβ) pathology becomes crucial in patients with clinically suspected Alzheimer's disease (AD). We evaluated Aβ levels in cerebrospinal fluid (Aβ CSF) and Aβ levels in positron emission tomography (Aβ PET) biomarkers in a real-world memory-clinic setting to develop an efficient algorithm for clinical use.
Methods: Patients were evaluated for AD-related Aβ pathology from two independent cohorts (Ludwig Maximilian University [LMU], = 402, and Medical University of Vienna [MUV], = 144).
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