Apparently, the job of a PhD is quite stressful, a recent study says.
A new study, published on Nature Communications by prof. Marcello D'Amelio's research group (Santa Lucia Foundation/Campus Bio-Medico, Rome), unveils new insights on the pathogenesis of Alzheimer's disease and opens new diagnostic perspectives.
Dr Panayiota Poirazi, chair of the FENS-Kavli Network of Excellence, analyzes the problems that european early- and mid-career scientists must face everyday as they try to obtain research funds, also suggesting the mechanisms of grant application and evaluation that funding agencies should improve to help young scientists build a career.
La Fondazione italiana sclerosi multipla ha pubblicato il Bando FISM 2017 per il finanziamento di progetti di ricerca e borse di studio sulla sclerosi multipla.
In this review, recently published on Science, Dr. Jonathan Kipnis summarizes the cellular and molecular mechanisms behind the role of lymphocytes in inducing and modulating immune tolerance in the CNS, with particular attention to the trafficking of immune cells and solubile factors throughout the meningeal lymphatic vessels and peripheral deep cervical lymph nodes.
L’importante finanziamento assegnato al neurologo Gianvito Martino (San Raffaele) per un progetto di ricerca che coinvolge laboratori tra Europa, Stati Uniti e Canada
Tissue-resident memory T cells (TRM) persist at sites of prior infection and have been shown to enhance pathogen clearance by recruiting circulating immune cells and providing bystander activation. Here, we characterize the functioning of brain-resident memory T cells (bTRM) in an animal model of viral infection...
J Exp Med.; 2016
A newly updated map of the human brain may be the most accurate yet, helping solve over 100 years of arguments.
Nature; August 2016
Myasthenia gravis (MG) is a chronic autoimmune disease characterized by fluctuating muscle weakness, which, in the majority of patients, is treated with corticosteroids. In a recently published clinical trial, 50 patients with generalized MG were randomly assigned to prednisone + methotrexate or prednisone + placebo. The amount of prednisone that…
Motor neurons are the final stage of neural processing for the execution of motor behaviours. Traditionally, motor neurons have been viewed as the ‘final common pathway’, serving as passive recipients merely conveying to the muscles the final motor program generated by upstream interneuron circuits1, 2. Here we reveal an unforeseen role of motor neurons in controlling the locomotor circuit function via gap junctions in zebrafish. These gap junctions mediate a retrograde analogue propagation of voltage fluctuations from motor neurons to control the synaptic release and recruitment of the upstream V2a interneurons that drive locomotion. Selective inhibition of motor neurons during ongoing locomotion de-recruits V2a interneurons and strongly influences locomotor circuit function. Rather than acting as separate units, gap junctions unite motor neurons and V2a interneurons into functional ensembles endowed with a retrograde analogue computation essential for locomotor rhythm generation. These results show that motor neurons are not a passive recipient of motor commands but an integral component of the neural circuits responsible for motor behaviour.
Glutamate receptors form complexes in the brain with auxiliary proteins, which control their activity during fast synaptic transmission through a seemingly bewildering array of effects. Here we devise a way to isolate the activation of complexes using polyamines, which enables us to show that transmembrane AMPA receptor regulatory proteins (TARPs) exert their effects principally on the channel opening reaction. A thermodynamic argument suggests that because TARPs promote channel opening, receptor activation promotes AMPAR-TARP complexes into a superactive state with high open probability. A simple model based on this idea predicts all known effects of TARPs on AMPA receptor function. This model also predicts unexpected phenomena including massive potentiation in the absence of desensitization and supramaximal recovery that we subsequently detected in electrophysiological recordings. This transient positive feedback mechanism has implications for information processing in the brain, because it should allow activity-dependent facilitation of excitatory synaptic transmission through a postsynaptic mechanism.
Social cognition enables individuals to understand others' intentions. Social memory is a necessary component of this process, for without it, subsequent encounters are devoid of any historical information. The CA2 area of the hippocampus, particularly the vasopressin 1b receptor (Avpr1b) expressed there, is necessary for memory formation. We used optogenetics to excite vasopressin terminals, originating from the hypothalamic paraventricular nucleus, in the CA2 of mice. This markedly enhanced their social memory if the stimulation occurred during memory acquisition, but not retrieval. This effect was blocked by an Avpr1b antagonist. Finally, this enhanced memory is resistant to the social distraction of an introduced second mouse, important for socially navigating populations of individuals. Our results indicate the CA2 can increase the salience of social signals. Targeted pharmacotherapy with Avpr1b agonists or deep brain stimulation of the CA2 are potential avenues of treatment for those with declining social memory as in various dementias.
Microglia are integral functional elements of the central nervous system, but the contribution of these cells to the structural integrity of the neurovascular unit has not hitherto been assessed. We show here that following blood–brain barrier (BBB) breakdown, P2RY12 (purinergic receptor P2Y, G-protein coupled, 12)-mediated chemotaxis of microglia processes is required for the rapid closure of the BBB. Mice treated with the P2RY12 inhibitor clopidogrel, as well as those in which P2RY12 was genetically ablated, exhibited significantly diminished movement of juxtavascular microglial processes and failed to close laser-induced openings of the BBB. Thus, microglial cells play a previously unrecognized protective role in the maintenance of BBB integrity following cerebrovascular damage. Because clopidogrel antagonizes the platelet P2Y12 receptor, it is widely prescribed for patients with coronary artery and cerebrovascular disease. As such, these observations suggest the need for caution in the postincident continuation of P2RY12-targeted platelet inhibition.