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Brain: a Journal of Neurology

Stéphane Prange, Javier Pagonabarraga, Paul Krack, Jaime Kulisevsky, Véronique Sgambato, Léon Tremblay, Stéphane Thobois, Emmanuel Broussolle
No abstract text is available yet for this article.
January 9, 2018: Brain: a Journal of Neurology
Erika Bereczki, Rui M Branca, Paul T Francis, Joana B Pereira, Jean-Ha Baek, Tibor Hortobágyi, Bengt Winblad, Clive Ballard, Janne Lehtiö, Dag Aarsland
Cognitive changes occurring throughout the pathogenesis of neurodegenerative diseases are directly linked to synaptic loss. We used in-depth proteomics to compare 32 post-mortem human brains in the prefrontal cortex of prospectively followed patients with Alzheimer's disease, Parkinson's disease with dementia, dementia with Lewy bodies and older adults without dementia. In total, we identified 10 325 proteins, 851 of which were synaptic proteins. Levels of 25 synaptic proteins were significantly altered in the various dementia groups...
January 9, 2018: Brain: a Journal of Neurology
Michal T Kucewicz, Brent M Berry, Laura R Miller, Fatemeh Khadjevand, Youssef Ezzyat, Joel M Stein, Vaclav Kremen, Benjamin H Brinkmann, Paul Wanda, Michael R Sperling, Richard Gorniak, Kathryn A Davis, Barbara C Jobst, Robert E Gross, Bradley Lega, Jamie Van Gompel, S Matt Stead, Daniel S Rizzuto, Michael J Kahana, Gregory A Worrell
Direct electrical stimulation of the human brain can elicit sensory and motor perceptions as well as recall of memories. Stimulating higher order association areas of the lateral temporal cortex in particular was reported to activate visual and auditory memory representations of past experiences (Penfield and Perot, 1963). We hypothesized that this effect could be used to modulate memory processing. Recent attempts at memory enhancement in the human brain have been focused on the hippocampus and other mesial temporal lobe structures, with a few reports of memory improvement in small studies of individual brain regions...
January 8, 2018: Brain: a Journal of Neurology
Tom A Vale, Mkael Symmonds, Michael Polydefkis, Kelly Byrnes, Andrew S C Rice, Andreas C Themistocleous, David L H Bennett
No abstract text is available yet for this article.
January 5, 2018: Brain: a Journal of Neurology
Merle C Hoenig, Gérard N Bischof, Joseph Seemiller, Jochen Hammes, Juraj Kukolja, Özgür A Onur, Frank Jessen, Klaus Fliessbach, Bernd Neumaier, Gereon R Fink, Thilo van Eimeren, Alexander Drzezga
A stereotypical anatomical propagation of tau pathology has been described in Alzheimer's disease. According to recent concepts (network degeneration hypothesis), this propagation is thought to be indicative of misfolded tau proteins possibly spreading along functional networks. If true, tau pathology accumulation should correlate in functionally connected brain regions. Therefore, we examined whether independent components could be identified in the distribution pattern of in vivo tau pathology and whether these components correspond with specific functional connectivity networks...
January 5, 2018: Brain: a Journal of Neurology
Clare M Eglin, Hugh Montgomery, Michael J Tipton
No abstract text is available yet for this article.
January 5, 2018: Brain: a Journal of Neurology
Nils Richter, Nora Beckers, Oezguer A Onur, Markus Dietlein, Marc Tittgemeyer, Lutz Kracht, Bernd Neumaier, Gereon R Fink, Juraj Kukolja
In early Alzheimer's disease, which initially presents with progressive loss of short-term memory, neurodegeneration especially affects cholinergic neurons of the basal forebrain. Pharmacotherapy of Alzheimer's disease therefore often targets the cholinergic system. In contrast, cholinergic pharmacotherapy of mild cognitive impairment is debated since its efficacy to date remains controversial. We here investigated the relationship between cholinergic treatment effects and the integrity of the cholinergic system in mild cognitive impairment due to Alzheimer's disease...
January 4, 2018: Brain: a Journal of Neurology
James H Cole, Amy Jolly, Sara de Simoni, Niall Bourke, Maneesh C Patel, Gregory Scott, David J Sharp
Traumatic brain injury leads to significant loss of brain volume, which continues into the chronic stage. This can be sensitively measured using volumetric analysis of MRI. Here we: (i) investigated longitudinal patterns of brain atrophy; (ii) tested whether atrophy is greatest in sulcal cortical regions; and (iii) showed how atrophy could be used to power intervention trials aimed at slowing neurodegeneration. In 61 patients with moderate-severe traumatic brain injury (mean age = 41.55 years ± 12.77) and 32 healthy controls (mean age = 34...
January 4, 2018: Brain: a Journal of Neurology
Remika Mito, David Raffelt, Thijs Dhollander, David N Vaughan, J-Donald Tournier, Olivier Salvado, Amy Brodtmann, Christopher C Rowe, Victor L Villemagne, Alan Connelly
Alzheimer's disease is increasingly considered a large-scale network disconnection syndrome, associated with progressive aggregation of pathological proteins, cortical atrophy, and functional disconnections between brain regions. These pathological changes are posited to arise in a stereotypical spatiotemporal manner, targeting intrinsic networks in the brain, most notably the default mode network. While this network-specific disruption has been thoroughly studied with functional neuroimaging, changes to specific white matter fibre pathways within the brain's structural networks have not been closely investigated, largely due to the challenges of modelling complex white matter structure...
January 4, 2018: Brain: a Journal of Neurology
Thomas E Cope, Timothy Rittman, Robin J Borchert, P Simon Jones, Deniz Vatansever, Kieren Allinson, Luca Passamonti, Patricia Vazquez Rodriguez, W Richard Bevan-Jones, John T O'Brien, James B Rowe
No abstract text is available yet for this article.
December 26, 2017: Brain: a Journal of Neurology
Derek B Archer, Stephen A Coombes, Winston T Chu, Jae Woo Chung, Roxana G Burciu, Michael S Okun, Aparna Wagle Shukla, David E Vaillancourt
Essential tremor is a neurological syndrome of heterogeneous pathology and aetiology that is characterized by tremor primarily in the upper extremities. This tremor is commonly hypothesized to be driven by a single or multiple neural oscillator(s) within the cerebello-thalamo-cortical pathway. Several studies have found an association of blood-oxygen level-dependent (BOLD) signal in the cerebello-thalamo-cortical pathway with essential tremor, but there is behavioural evidence that also points to the possibility that the severity of tremor could be influenced by visual feedback...
December 22, 2017: Brain: a Journal of Neurology
Nadia Giordano, Attilio Iemolo, Maria Mancini, Fabrizio Cacace, Maria De Risi, Emanuele Claudio Latagliata, Veronica Ghiglieri, Gian Carlo Bellenchi, Stefano Puglisi-Allegra, Paolo Calabresi, Barbara Picconi, Elvira De Leonibus
Nigro-striatal dopamine transmission is central to a wide range of neuronal functions, including skill learning, which is disrupted in several pathologies such as Parkinson's disease. The synaptic plasticity mechanisms, by which initial motor learning is stored for long time periods in striatal neurons, to then be gradually optimized upon subsequent training, remain unexplored. Addressing this issue is crucial to identify the synaptic and molecular mechanisms involved in striatal-dependent learning impairment in Parkinson's disease...
December 21, 2017: Brain: a Journal of Neurology
Gregory Scott, Henrik Zetterberg, Amy Jolly, James H Cole, Sara De Simoni, Peter O Jenkins, Claire Feeney, David R Owen, Anne Lingford-Hughes, Oliver Howes, Maneesh C Patel, Anthony P Goldstone, Roger N Gunn, Kaj Blennow, Paul M Matthews, David J Sharp
Survivors of a traumatic brain injury can deteriorate years later, developing brain atrophy and dementia. Traumatic brain injury triggers chronic microglial activation, but it is unclear whether this is harmful or beneficial. A successful chronic-phase treatment for traumatic brain injury might be to target microglia. In experimental models, the antibiotic minocycline inhibits microglial activation. We investigated the effect of minocycline on microglial activation and neurodegeneration using PET, MRI, and measurement of the axonal protein neurofilament light in plasma...
December 19, 2017: Brain: a Journal of Neurology
Michael Sommerauer, Tatyana D Fedorova, Allan K Hansen, Karoline Knudsen, Marit Otto, Jesper Jeppesen, Yoon Frederiksen, Jakob U Blicher, Jacob Geday, Adjmal Nahimi, Malene F Damholdt, David J Brooks, Per Borghammer
Pathological involvement of the noradrenergic locus coeruleus occurs early in Parkinson's disease, and widespread noradrenaline reductions are found at post-mortem. Rapid eye movement sleep behaviour disorder (RBD) accompanies Parkinson's disease and its presence predicts an unfavourable disease course with a higher propensity to cognitive impairment and orthostatic hypotension. MRI can detect neuromelanin in the locus coeruleus while 11C-MeNER PET is a marker of noradrenaline transporter availability. Here, we use both imaging modalities to study the association of RBD, cognition and autonomic dysfunction in Parkinson's disease with loss of noradrenergic function...
December 18, 2017: Brain: a Journal of Neurology
Julia Thompson, Mian Bi, Andrew G Murchison, Mateusz Makuch, Christian G Bien, Kon Chu, Pue Farooque, Jeffrey M Gelfand, Michael D Geschwind, Lawrence J Hirsch, Ernest Somerville, Bethan Lang, Angela Vincent, Maria I Leite, Patrick Waters, Sarosh R Irani
Faciobrachial dystonic seizures and limbic encephalitis closely associate with antibodies to leucine-rich glioma-inactivated 1 (LGI1). Here, we describe 103 consecutive patients with faciobrachial dystonic seizures and LGI1 antibodies to understand clinical, therapeutic and serological differences between those with and without cognitive impairment, and to determine whether cessation of faciobrachial dystonic seizures can prevent cognitive impairment. The 22/103 patients without cognitive impairment typically had normal brain MRI, EEGs and serum sodium levels (P < 0...
December 18, 2017: Brain: a Journal of Neurology
Izumi Maezawa, Hai M Nguyen, Jacopo Di Lucente, David Paul Jenkins, Vikrant Singh, Silvia Hilt, Kyoungmi Kim, Srikant Rangaraju, Allan I Levey, Heike Wulff, Lee-Way Jin
Microglia significantly contribute to the pathophysiology of Alzheimer's disease but an effective microglia-targeted therapeutic approach is not yet available clinically. The potassium channels Kv1.3 and Kir2.1 play important roles in regulating immune cell functions and have been implicated by in vitro studies in the 'M1-like pro-inflammatory' or 'M2-like anti-inflammatory' state of microglia, respectively. We here found that amyloid-β oligomer-induced expression of Kv1.3 and Kir2.1 in cultured primary microglia...
December 18, 2017: Brain: a Journal of Neurology
Marie d'Orange, Gwénaelle Aurégan, Dimitri Cheramy, Mylène Gaudin-Guérif, Sarah Lieger, Martine Guillermier, Lev Stimmer, Charlène Joséphine, Anne-Sophie Hérard, Marie-Claude Gaillard, Fanny Petit, Maren Christine Kiessling, Christoph Schmitz, Morvane Colin, Luc Buée, Fany Panayi, Elsa Diguet, Emmanuel Brouillet, Philippe Hantraye, Alexis-Pierre Bemelmans, Karine Cambon
Tauopathies are neurodegenerative diseases characterized by the aggregation of tau protein. These pathologies exhibit a wide variety of clinical and anatomo-pathological presentations, which may result from different pathological mechanisms. Although tau inclusions are a common feature in all these diseases, recent evidence instead implicates small oligomeric aggregates as drivers of tau-induced toxicity. Hence in vivo model systems displaying either soluble or fibrillary forms of wild-type or mutant tau are needed to better identify their respective pathological pathways...
December 14, 2017: Brain: a Journal of Neurology
Olesya Grinenko, Jian Li, John C Mosher, Irene Z Wang, Juan C Bulacio, Jorge Gonzalez-Martinez, Dileep Nair, Imad Najm, Richard M Leahy, Patrick Chauvel
Defining a bio-electrical marker for the brain area responsible for initiating a seizure remains an unsolved problem. Fast gamma activity has been identified as the most specific marker for seizure onset, but conflicting results have been reported. In this study, we describe an alternative marker, based on an objective description of interictal to ictal transition, with the aim of identifying a time-frequency pattern or 'fingerprint' that can differentiate the epileptogenic zone from areas of propagation. Seventeen patients who underwent stereoelectroencephalography were included in the study...
December 14, 2017: Brain: a Journal of Neurology
Abdella M Habib, Ayako Matsuyama, Andrei L Okorokov, Sonia Santana-Varela, Jose T Bras, Anna Maria Aloisi, Edward C Emery, Yury D Bogdanov, Maryne Follenfant, Sam J Gossage, Mathilde Gras, Jack Humphrey, Anna Kolesnikov, Kim Le Cann, Shengnan Li, Michael S Minett, Vanessa Pereira, Clara Ponsolles, Shafaq Sikandar, Jesus M Torres, Kenji Yamaoka, Jing Zhao, Yuriko Komine, Tetsuo Yamamori, Nikolas Maniatis, Konstantin I Panov, Henry Houlden, Juan D Ramirez, David L H Bennett, Letizia Marsili, Valeria Bachiocco, John N Wood, James J Cox
Chronic pain is a major global public health issue causing a severe impact on both the quality of life for sufferers and the wider economy. Despite the significant clinical burden, little progress has been made in terms of therapeutic development. A unique approach to identifying new human-validated analgesic drug targets is to study rare families with inherited pain insensitivity. Here we have analysed an otherwise normal family where six affected individuals display a pain insensitive phenotype that is characterized by hyposensitivity to noxious heat and painless bone fractures...
December 14, 2017: Brain: a Journal of Neurology
Shelley L Forrest, Jillian J Kril, Claire H Stevens, John B Kwok, Marianne Hallupp, Woojin S Kim, Yue Huang, Ciara V McGinley, Hellen Werka, Matthew C Kiernan, Jürgen Götz, Maria Grazia Spillantini, John R Hodges, Lars M Ittner, Glenda M Halliday
In many neurodegenerative disorders, familial forms have provided important insights into the pathogenesis of their corresponding sporadic forms. The first mutations associated with frontotemporal lobar degeneration (FTLD) were found in the microtubule-associated protein tau (MAPT) gene on chromosome 17 in families with frontotemporal degeneration and parkinsonism (FTDP-17). However, it was soon discovered that 50% of these families had a nearby mutation in progranulin. Regardless, the original FTDP-17 nomenclature has been retained for patients with MAPT mutations, with such patients currently classified independently from the different sporadic forms of FTLD with tau-immunoreactive inclusions (FTLD-tau)...
December 14, 2017: Brain: a Journal of Neurology
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