TY  - JOUR
AU  - Mäkinen, E.E.
AU  - Lensu, S.
AU  - Wikgren, J.
AU  - Pekkala, S.
AU  - Koch, L.G.
AU  - Britton, S.L.
AU  - Nokia, M.S.
TI  - Intrinsic running capacity associates with hippocampal electrophysiology and long-term potentiation in rats
JF  - NEUROSCIENCE LETTERS
J2  - NEUROSCI LETT
VL  - 823
PY  - 2024
SN  - 0304-3940
DO  - 10.1016/j.neulet.2024.137665
UR  - https://m2.mtmt.hu/api/publication/34759393
ID  - 34759393
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Contreras, Ana
AU  - Djebari, Souhail
AU  - Temprano-Carazo, Sara
AU  - Munera, Alejandro
AU  - Gruart, Agnes
AU  - Delgado-Garcia, Jose M.
AU  - Jimenez-Diaz, Lydia
AU  - Navarro-Lopez, Juan D.
TI  - Impairments in hippocampal oscillations accompany the loss of LTP induced by GIRK activity blockade
JF  - NEUROPHARMACOLOGY
J2  - NEUROPHARMACOLOGY
VL  - 238
PY  - 2023
PG  - 9
SN  - 0028-3908
DO  - 10.1016/j.neuropharm.2023.109668
UR  - https://m2.mtmt.hu/api/publication/34280745
ID  - 34280745
AB  - Learning and memory occurrence requires of hippocampal long-term synaptic plasticity and precise neural activity orchestrated by brain network oscillations, both processes reciprocally influencing each other. As G-protein-gated inwardly rectifying potassium (GIRK) channels rule synaptic plasticity that supports hippocampaldependent memory, here we assessed their unknown role in hippocampal oscillatory activity in relation to synaptic plasticity induction.In alert male mice, pharmacological GIRK modulation did not alter neural oscillations before long-term potentiation (LTP) induction. However, after an LTP generating protocol, both gain- and loss-of basal GIRK activity transformed LTP into long-term depression, but only specific suppression of constitutive GIRK activity caused a disruption of network synchronization (6, & alpha;, & gamma; bands), even leading to long-lasting ripples and fast ripples pathological oscillations. Together, our data showed that constitutive GIRK activity plays a key role in the tuning mechanism of hippocampal oscillatory activity during long-term synaptic plasticity processes that underlies hippocampaldependent cognitive functions.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Victorino, D.B.
AU  - Faber, J.
AU  - Pinheiro, D.J.L.L.
AU  - Scorza, F.A.
AU  - Almeida, A.C.G.
AU  - Costa, A.C.S.
AU  - Scorza, C.A.
TI  - Toward the Identification of Neurophysiological Biomarkers for Alzheimer's Disease in Down Syndrome: A Potential Role for Cross-Frequency Phase-Amplitude Coupling Analysis
JF  - AGING AND DISEASE
J2  - AGING DIS
VL  - 14
PY  - 2023
IS  - 2
SP  - 428
EP  - 449
PG  - 22
SN  - 2152-5250
DO  - 10.14336/AD.2022.0906
UR  - https://m2.mtmt.hu/api/publication/34114129
ID  - 34114129
AB  - Cross-frequency coupling (CFC) mechanisms play a central role in brain activity. Pathophysiological mechanisms leading to many brain disorders, such as Alzheimer's disease (AD), may produce unique patterns of brain activity detectable by electroencephalography (EEG). Identifying biomarkers for AD diagnosis is also an ambition among research teams working in Down syndrome (DS), given the increased susceptibility of people with DS to develop early-onset AD (DS-AD). Here, we review accumulating evidence that altered theta-gamma phase-amplitude coupling (PAC) may be one of the earliest EEG signatures of AD, and therefore may serve as an adjuvant tool for detecting cognitive decline in DS-AD. We suggest that this field of research could potentially provide clues to the biophysical mechanisms underlying cognitive dysfunction in DS-AD and generate opportunities for identifying EEG-based biomarkers with diagnostic and prognostic utility in DS-AD. Copyright: © 2022 Victorino DB. et al.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Datki, Zsolt László
AU  - Balázs, Evelin
AU  - Gálik, Bence
AU  - Sinka, Rita
AU  - Zeitler, Lavínia
AU  - Bozsó, Zsolt
AU  - Kálmán, János
AU  - Hortobágyi, Tibor
AU  - Oláh, Zita
TI  - The interacting rotifer-biopolymers are anti- and disaggregating agents for human-type beta-amyloid in vitro
JF  - INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
J2  - INT J BIOL MACROMOL
VL  - 201
PY  - 2022
SP  - 262
EP  - 269
PG  - 8
SN  - 0141-8130
DO  - 10.1016/j.ijbiomac.2021.12.184
UR  - https://m2.mtmt.hu/api/publication/32591465
ID  - 32591465
N1  - Funding Agency and Grant Number: Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences; New National Excellence Program of the Ministry for Innovation and Technology from the source of the National Research, Development and Innovation Found [UNKP-21-5-SZTE-555]; European Union [754432]; Polish Ministry of Science and Higher Education; SZTEAOK-KKA [5S 567 (A202)]; Developing Scientific Workshops of Medical-, Health Sciences and Pharmaceutical Training (Hungary) [EFOP 3.6.3-VEKOP-16-201700009]
            Funding text: This project was supported by the J ' anos Bolyai Research Scholarship of the Hungarian Academy of Sciences; by the UNKP-21-5-SZTE-555 New National Excellence Program of the Ministry for Innovation and Technology from the source of the National Research, Development and Innovation Found; by the European Union's Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie grant agreement, Nr. 754432; by the Polish Ministry of Science and Higher Education; by the SZTE ' AOK-KKA No. 5S 567 (A202) and by the Developing Scientific Workshops of Medical-, Health Sciences and Pharmaceutical Training (grant number: EFOP 3.6.3-VEKOP-16-201700009; Hungary).
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Leparulo, A.
AU  - Bisio, M.
AU  - Redolfi, N.
AU  - Pozzan, T.
AU  - Vassanelli, S.
AU  - Fasolato, C.
TI  - Accelerated Aging Characterizes the Early Stage of Alzheimer’s Disease
JF  - CELLS
J2  - CELLS-BASEL
VL  - 11
PY  - 2022
IS  - 2
PG  - 21
SN  - 2073-4409
DO  - 10.3390/cells11020238
UR  - https://m2.mtmt.hu/api/publication/32640861
ID  - 32640861
AB  - For Alzheimer’s disease (AD), aging is the main risk factor, but whether cognitive impairments due to aging resemble early AD deficits is not yet defined. When working with mouse models of AD, the situation is just as complicated, because only a few studies track the progression of the disease at different ages, and most ignore how the aging process affects control mice. In this work, we addressed this problem by comparing the aging process of PS2APP (AD) and wild-type (WT) mice at the level of spontaneous brain electrical activity under anesthesia. Using local field potential recordings, obtained with a linear probe that traverses the posterior parietal cortex and the entire hippocampus, we analyzed how multiple electrical parameters are modified by aging in AD and WT mice. With this approach, we highlighted AD specific features that appear in young AD mice prior to plaque deposition or that are delayed at 12 and 16 months of age. Furthermore, we identified aging characteristics present in WT mice but also occurring prematurely in young AD mice. In short, we found that reduction in the relative power of slow oscillations (SO) and Low/High power imbalance are linked to an AD phenotype at its onset. The loss of SO connectivity and cortico-hippocampal coupling between SO and higher frequencies as well as the increase in UP-state and burst durations are found in young AD and old WT mice. We show evidence that the aging process is accelerated by the mutant PS2 itself and discuss such changes in relation to amyloidosis and gliosis. © 2022 by the authors. Licensee MDPI, Basel, Switzerland.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Andrade-Talavera, Yuniesky
AU  - Rodriguez-Moreno, Antonio
TI  - Synaptic Plasticity and Oscillations in Alzheimer's Disease: A Complex Picture of a Multifaceted Disease
JF  - FRONTIERS IN MOLECULAR NEUROSCIENCE
J2  - FRONT MOL NEUROSCI
VL  - 14
PY  - 2021
PG  - 10
SN  - 1662-5099
DO  - 10.3389/fnmol.2021.696476
UR  - https://m2.mtmt.hu/api/publication/32287233
ID  - 32287233
AB  - Brain plasticity is widely accepted as the core neurophysiological basis of memory and is generally defined by activity-dependent changes in synaptic efficacy, such as long-term potentiation (LTP) and long-term depression (LTD). By using diverse induction protocols like high-frequency stimulation (HFS) or spike-timing dependent plasticity (STDP), such crucial cognition-relevant plastic processes are shown to be impaired in Alzheimer's disease (AD). In AD, the severity of the cognitive impairment also correlates with the level of disruption of neuronal network dynamics. Currently under debate, the named amyloid hypothesis points to amyloid-beta peptide 1-42 (A beta 42) as the trigger of the functional deviations underlying cognitive impairment in AD. However, there are missing functional mechanistic data that comprehensively dissect the early subtle changes that lead to synaptic dysfunction and subsequent neuronal network collapse in AD. The convergence of the study of both, mechanisms underlying brain plasticity, and neuronal network dynamics, may represent the most efficient approach to address the early triggering and aberrant mechanisms underlying the progressive clinical cognitive impairment in AD. Here we comment on the emerging integrative roles of brain plasticity and network oscillations in AD research and on the future perspectives of research in this field.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Isla, Arturo G.
AU  - Balleza-Tapia, Hugo
AU  - Fisahn, Andre
TI  - Efficacy of preclinical pharmacological interventions against alterations of neuronal network oscillations in Alzheimer's disease: A systematic review
JF  - EXPERIMENTAL NEUROLOGY
J2  - EXP NEUROL
VL  - 343
PY  - 2021
PG  - 14
SN  - 0014-4886
DO  - 10.1016/j.expneurol.2021.113743
UR  - https://m2.mtmt.hu/api/publication/32286384
ID  - 32286384
AB  - Despite the development of multiple pharmacological approaches over the years aimed at treating Alzheimer's Disease (AD) only very few have been approved for clinical use in patients. To date there still exists no diseasemodifying treatment that could prevent or rescue the cognitive impairment, particularly of memory aquisition, that is characteristic of AD. One of the possibilities for this state of affairs might be that the majority of drug discovery efforts focuses on outcome measures of decreased neuropathological biomarkers characteristic of AD, without taking into acount neuronal processes essential to the generation and maintenance of memory processes. Particularly, the capacity of the brain to generate theta (theta) and gamma (gamma) oscillatory activity has been strongly correlated to memory performance. Using a systematic review approach, we synthesize the existing evidence in the literature on pharmacological interventions that enhance neuronal theta (theta) and/or gamma (gamma) oscillations in non-pathological animal models and in AD animal models. Additionally, we synthesize the main outcomes and neurochemical systems targeted. We propose that functional biomarkers such as cognition-relevant neuronal network oscillations should be used as outcome measures during the process of research and development of novel drugs against cognitive impairment in AD.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Sudkamp, Nicolina
AU  - Shchyglo, Olena
AU  - Manahan-Vaughan, Denise
TI  - Absence of Pannexin 1 Stabilizes Hippocampal Excitability After Intracerebral Treatment With A beta (1-42) and Prevents LTP Deficits in Middle-Aged Mice
JF  - FRONTIERS IN AGING NEUROSCIENCE
J2  - FRONT AGING NEUROSCI
VL  - 13
PY  - 2021
PG  - 16
SN  - 1663-4365
DO  - 10.3389/fnagi.2021.591735
UR  - https://m2.mtmt.hu/api/publication/32337186
ID  - 32337186
AB  - Beta-amyloid protein [A beta(1-42)] plays an important role in the disease progress and pathophysiology of Alzheimer's disease (AD). Membrane properties and neuronal excitability are altered in the hippocampus of transgenic AD mouse models that overexpress amyloid precursor protein. Although gap junction hemichannels have been implicated in the early pathogenesis of AD, to what extent Pannexin channels contribute to A beta(1-42)-mediated brain changes is not yet known. In this study we, therefore, investigated the involvement of Pannexin1 (Panx1) channels in A beta-mediated changes of neuronal membrane properties and long-term potentiation (LTP) in an animal model of AD. We conducted whole-cell patch-clamp recordings in CA1 pyramidal neurons 1 week after intracerebroventricular treatments of adult wildtype (wt) and Panx1 knockout (Panx1-ko) mice with either oligomeric A beta(1-42), or control peptide. Panx1-ko hippocampi treated with control peptide exhibited increased neuronal excitability compared to wt. In addition, action potential (AP) firing frequency was higher in control Panx1-ko slices compared to wt. A beta-treatment reduced AP firing frequency in both cohorts. But in A beta-treated wt mice, spike frequency adaptation was significantly enhanced, when compared to control wt and to A beta-treated Panx1-ko mice. Assessment of hippocampal LTP revealed deficits in A beta-treated wt compared to control wt. By contrast, Panx1-ko exhibited LTP that was equivalent to LTP in control ko hippocampi. Taken together, our data show that in the absence of Pannexin1, hippocampi are more resistant to the debilitating effects of oligomeric A beta. Both A beta-mediated impairments in spike frequency adaptation and in LTP that occur in wt animals, are ameliorated in Panx1-ko mice. These results suggest that Panx1 contributes to early changes in hippocampal neuronal and synaptic function that are triggered by oligomeric A beta.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Babiloni, C.
AU  - Blinowska, K.
AU  - Bonanni, L.
AU  - Cichocki, A.
AU  - De, Haan W.
AU  - Del, Percio C.
AU  - Dubois, B.
AU  - Escudero, J.
AU  - Fernández, A.
AU  - Frisoni, G.
AU  - Guntekin, B.
AU  - Hajos, M.
AU  - Hampel, H.
AU  - Ifeachor, E.
AU  - Kilborn, K.
AU  - Kumar, S.
AU  - Johnsen, K.
AU  - Johannsson, M.
AU  - Jeong, J.
AU  - LeBeau, F.
AU  - Lizio, R.
AU  - Lopes, da Silva F.
AU  - Maestú, F.
AU  - McGeown, W.J.
AU  - McKeith, I.
AU  - Moretti, D.V.
AU  - Nobili, F.
AU  - Olichney, J.
AU  - Onofrj, M.
AU  - Palop, J.J.
AU  - Rowan, M.
AU  - Stocchi, F.
AU  - Struzik, Z.M.
AU  - Tanila, H.
AU  - Teipel, S.
AU  - Taylor, J.P.
AU  - Weiergräber, M.
AU  - Yener, G.
AU  - Young-Pearse, T.
AU  - Drinkenburg, W.H.
AU  - Randall, F.
TI  - What electrophysiology tells us about Alzheimer's disease: a window into the synchronization and connectivity of brain neurons
JF  - NEUROBIOLOGY OF AGING: AGE-RELATED PHENOMENA NEURODEGENERATION AND NEUROPATHOLOGY
J2  - NEUROBIOL AGING
VL  - 85
PY  - 2020
SP  - 58
EP  - 73
PG  - 16
SN  - 0197-4580
DO  - 10.1016/j.neurobiolaging.2019.09.008
UR  - https://m2.mtmt.hu/api/publication/33264551
ID  - 33264551
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Balázs, Evelin
AU  - Oláh, Zita
AU  - Gálik, Bence
AU  - Bozsó, Zsolt
AU  - Kálmán, János
AU  - Datki, Zsolt László
TI  - Neurodegeneration-related beta-amyloid as autocatabolism-attenuator in a micro-in vivo system
JF  - IBRO REPORTS
J2  - IBRO REP
VL  - 9
PY  - 2020
SP  - 319
EP  - 323
PG  - 5
SN  - 2451-8301
DO  - 10.1016/j.ibror.2020.10.002
UR  - https://m2.mtmt.hu/api/publication/31639846
ID  - 31639846
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Chung, H.
AU  - Park, K.
AU  - Jang, H.J.
AU  - Kohl, M.M.
AU  - Kwag, J.
TI  - Dissociation of somatostatin and parvalbumin interneurons circuit dysfunctions underlying hippocampal theta and gamma oscillations impaired by amyloid β oligomers in vivo
JF  - BRAIN STRUCTURE & FUNCTION
J2  - BRAIN STRUCT FUNC
VL  - 225
PY  - 2020
IS  - 3
SP  - 935
EP  - 954
PG  - 20
SN  - 1863-2653
DO  - 10.1007/s00429-020-02044-3
UR  - https://m2.mtmt.hu/api/publication/31314638
ID  - 31314638
AB  - Accumulation of amyloid β oligomers (AβO) in Alzheimer’s disease (AD) impairs hippocampal theta and gamma oscillations. These oscillations are important in memory functions and depend on distinct subtypes of hippocampal interneurons such as somatostatin-positive (SST) and parvalbumin-positive (PV) interneurons. Here, we investigated whether AβO causes dysfunctions in SST and PV interneurons by optogenetically manipulating them during theta and gamma oscillations in vivo in AβO-injected SST-Cre or PV-Cre mice. Hippocampal in vivo multi-electrode recordings revealed that optogenetic activation of channelrhodopsin-2 (ChR2)-expressing SST and PV interneurons in AβO-injected mice selectively restored AβO-induced reduction of the peak power of theta and gamma oscillations, respectively, and resynchronized CA1 pyramidal cell (PC) spikes. Moreover, SST and PV interneuron spike phases were resynchronized relative to theta and gamma oscillations, respectively. Whole-cell voltage-clamp recordings in CA1 PC in ex vivo hippocampal slices from AβO-injected mice revealed that optogenetic activation of SST and PV interneurons enhanced spontaneous inhibitory postsynaptic currents (IPSCs) selectively at theta and gamma frequencies, respectively. Furthermore, analyses of the stimulus–response curve, paired-pulse ratio, and short-term plasticity of SST and PV interneuron-evoked IPSCs ex vivo showed that AβO increased the initial GABA release probability to depress SST/PV interneuron’s inhibitory input to CA1 PC selectively at theta and gamma frequencies, respectively. Our results reveal frequency-specific and interneuron subtype-specific presynaptic dysfunctions of SST and PV interneurons’ input to CA1 PC as the synaptic mechanisms underlying AβO-induced impairments of hippocampal network oscillations and identify them as potential therapeutic targets for restoring hippocampal network oscillations in early AD. © 2020, The Author(s).
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Gauthier-Umanã, C.
AU  - Munõz-Cabrera, J.
AU  - Valderrama, M.
AU  - Múnera, A.
AU  - Nava-Mesa, M.O.
TI  - Acute Effects of Two Different Species of Amyloid-β on Oscillatory Activity and Synaptic Plasticity in the Commissural CA3-CA1 Circuit of the Hippocampus
JF  - NEURAL PLASTICITY
J2  - NEURAL PLAST
VL  - 2020
PY  - 2020
PG  - 13
SN  - 2090-5904
DO  - 10.1155/2020/8869526
UR  - https://m2.mtmt.hu/api/publication/31939733
ID  - 31939733
AB  - Recent evidence indicates that soluble amyloid-β (Aβ) species induce imbalances in excitatory and inhibitory transmission, resulting in neural network functional impairment and cognitive deficits during early stages of Alzheimer's disease (AD). To evaluate the in vivo effects of two soluble Aβ species (Aβ25-35 and Aβ1-40) on commissural CA3-to-CA1 (cCA3-to-CA1) synaptic transmission and plasticity, and CA1 oscillatory activity, we used acute intrahippocampal microinjections in adult anaesthetized male Wistar rats. Soluble Aβ microinjection increased cCA3-to-CA1 synaptic variability without significant changes in synaptic efficiency. High-frequency CA3 stimulation was rendered inefficient by soluble Aβ intrahippocampal injection to induce long-term potentiation and to enhance synaptic variability in CA1, contrasting with what was observed in vehicle-injected subjects. Although soluble Aβ microinjection significantly increased the relative power of γ-band and ripple oscillations and significantly shifted the average vector of θ-to-γ phase-amplitude coupling (PAC) in CA1, it prevented θ-to-γ PAC shift induced by high-frequency CA3 stimulation, opposite to what was observed in vehicle-injected animals. These results provide further evidence that soluble Aβ species induce synaptic dysfunction causing abnormal synaptic variability, impaired long-term plasticity, and deviant oscillatory activity, leading to network activity derailment in the hippocampus. © 2020 Cécile Gauthier-Umanã et al.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Hamilton, H.K.
AU  - Roach, B.J.
AU  - Cavus, I.
AU  - Teyler, T.J.
AU  - Clapp, W.C.
AU  - Ford, J.M.
AU  - Tarakci, E.
AU  - Krystal, J.H.
AU  - Mathalon, D.H.
TI  - Impaired Potentiation of Theta Oscillations During a Visual Cortical Plasticity Paradigm in Individuals With Schizophrenia
JF  - FRONTIERS IN PSYCHIATRY
J2  - FRONT PSYCHIATRY
VL  - 11
PY  - 2020
PG  - 14
SN  - 1664-0640
DO  - 10.3389/fpsyt.2020.590567
UR  - https://m2.mtmt.hu/api/publication/34565241
ID  - 34565241
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Sánchez-Rodríguez, I.
AU  - Djebari, S.
AU  - Temprano-Carazo, S.
AU  - Vega-Avelaira, D.
AU  - Jiménez-Herrera, R.
AU  - Iborra-Lázaro, G.
AU  - Yajeya, J.
AU  - Jiménez-Díaz, L.
AU  - Navarro-López, J.D.
TI  - Hippocampal long-term synaptic depression and memory deficits induced in early amyloidopathy are prevented by enhancing G-protein-gated inwardly rectifying potassium channel activity
JF  - JOURNAL OF NEUROCHEMISTRY
J2  - J NEUROCHEM
VL  - 153
PY  - 2020
IS  - 3
SP  - 362
EP  - 376
PG  - 15
SN  - 0022-3042
DO  - 10.1111/jnc.14946
UR  - https://m2.mtmt.hu/api/publication/31290261
ID  - 31290261
AB  - Hippocampal synaptic plasticity disruption by amyloid-β (Aβ) peptides + thought to be responsible for learning and memory impairments in Alzheimer's disease (AD) early stage. Failures in neuronal excitability maintenance seems to be an underlying mechanism. G-protein-gated inwardly rectifying potassium (GirK) channels control neural excitability by hyperpolarization in response to many G-protein-coupled receptors activation. Here, in early in vitro and in vivo amyloidosis mouse models, we study whether GirK channels take part of the hippocampal synaptic plasticity impairments generated by Aβ1–42. In vitro electrophysiological recordings from slices showed that Aβ1–42 alters synaptic plasticity by switching high-frequency stimulation (HFS) induced long-term potentiation (LTP) to long-term depression (LTD), which led to in vivo hippocampal-dependent memory deficits. Remarkably, selective pharmacological activation of GirK channels with ML297 rescued both HFS-induced LTP and habituation memory from Aβ1–42 action. Moreover, when GirK channels were specifically blocked by Tertiapin-Q, their activation with ML297 failed to rescue LTP from the HFS-dependent LTD induced by Aβ1–42. On the other hand, the molecular analysis of the recorded slices by western blot showed that the expression of GIRK1/2 subunits, which form the prototypical GirK channel in the hippocampus, was not significantly regulated by Aβ1–42. However, immunohistochemical examination of our in vivo amyloidosis model showed Aβ1–42 to down-regulate hippocampal GIRK1 subunit expression. Together, our results describe an Aβ-mediated deleterious synaptic mechanism that modifies the induction threshold for hippocampal LTP/LTD and underlies memory alterations observed in amyloidosis models. In this scenario, GirK activation assures memory formation by preventing the transformation of HFS-induced LTP into LTD. (Figure presented.). © 2019 The Authors. Journal of Neurochemistry published by John Wiley & Sons Ltd on behalf of International Society for Neurochemistry
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Peña-Ortega, F.
TI  - Brain arrhythmias induced by amyloid beta and inflammation: Involvement in alzheimer’s disease and other inflammation-related pathologies
JF  - CURRENT ALZHEIMER RESEARCH
J2  - CURR ALZHEIMER RES
VL  - 16
PY  - 2019
IS  - 12
SP  - 1108
EP  - 1131
PG  - 24
SN  - 1567-2050
DO  - 10.2174/1567205017666191213162233
UR  - https://m2.mtmt.hu/api/publication/31239913
ID  - 31239913
AB  - A variety of neurological diseases, including Alzheimer’s disease (AD), involve amyloid beta (Aβ) accumulation and/or neuroinflammation, which can alter synaptic and neural circuit functions. Consequently, these pathological conditions induce changes in neural network rhythmic activity (brain arrhythmias), which affects many brain functions. Neural network rhythms are involved in information processing, storage and retrieval, which are essential for memory consolidation, executive functioning and sensory processing. Therefore, brain arrhythmias could have catastrophic effects on circuit function, underlying the symptoms of various neurological diseases. Moreover, brain arrhythmias can serve as biomarkers for a variety of brain diseases. The aim of this review is to provide evidence linking Aβ and inflammation to neural network dysfunction, focusing on alterations in brain rhythms and their impact on cognition and sensory processing. I reviewed the most common brain arrhythmias characterized in AD, in AD transgenic models and those induced by Aβ. In addition, I reviewed the modulations of brain rhythms in neuroinflammatory diseases and those induced by immunogens, interleukins and microglia. This review reveals that Aβ and inflammation produce a complex set of effects on neural network function, which are related to the induction of brain arrhythmias and hyperexcitability, both closely related to behavioral alterations. Understanding these brain arrhythmias can help to develop therapeutic strategies to halt or prevent these neural network alterations and treat not only the arrhythmias but also the symptoms of AD and other inflammation-related pathologies. © 2019 Bentham Science Publishers.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Sánchez-Rodríguez, I.
AU  - Gruart, A.
AU  - Delgado-García, J.M.
AU  - Jiménez-Díaz, L.
AU  - Navarro-López, J.D.
TI  - Role of girk channels in long-term potentiation of synaptic inhibition in an in vivo mouse model of early amyloid-β pathology
JF  - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
J2  - INT J MOL SCI
VL  - 20
PY  - 2019
IS  - 5
SN  - 1661-6596
DO  - 10.3390/ijms20051168
UR  - https://m2.mtmt.hu/api/publication/30775278
ID  - 30775278
AB  - Imbalances of excitatory/inhibitory synaptic transmission occur early in the pathogenesis of Alzheimer’s disease (AD), leading to hippocampal hyperexcitability and causing synaptic, network, and cognitive dysfunctions. G-protein-gated potassium (GirK) channels play a key role in the control of neuronal excitability, contributing to inhibitory signaling. Here, we evaluate the relationship between GirK channel activity and inhibitory hippocampal functionality in vivo. In a non-transgenic mouse model of AD, field postsynaptic potentials (fPSPs) from the CA3–CA1 synapse in the dorsal hippocampus were recorded in freely moving mice. Intracerebroventricular (ICV) injections of amyloid-β (Aβ) or GirK channel modulators impaired ionotropic (GABAA-mediated fPSPs) and metabotropic (GirK-mediated fPSPs) inhibitory signaling and disrupted the potentiation of synaptic inhibition. However, the activation of GirK channels prevented Aβ-induced changes in GABAA components. Our data shows, for the first time, the presence of long-term potentiation (LTP) for both the GABAA and GirK-mediated inhibitory postsynaptic responses in vivo. In addition, our results support the importance of an accurate level of GirK-dependent signaling for dorsal hippocampal performance in early amyloid pathology models by controlling the excess of excitation that disrupts synaptic plasticity processes. © 2019 by the authors. Licensee MDPI, Basel, Switzerland.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Datki, Zsolt László
AU  - Oláh, Zita
AU  - Hortobágyi, Tibor
AU  - Borbélyné Mácsai, Lilla
AU  - Zsuga, Katalin
AU  - Fülöp, Lívia
AU  - Bozsó, Zsolt
AU  - Gálik, Bence
AU  - Ács, Éva
AU  - Földi, Angéla
AU  - Szarvas, A
AU  - Kálmán, János
TI  - Exceptional in vivo catabolism of neurodegeneration-related aggregates
JF  - ACTA NEUROPATHOLOGICA COMMUNICATIONS
J2  - ACTA NEUROPATH COMM
VL  - 6
PY  - 2018
IS  - 1
PG  - 12
SN  - 2051-5960
DO  - 10.1186/s40478-018-0507-3
UR  - https://m2.mtmt.hu/api/publication/3323000
ID  - 3323000
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Tamura, Hideki
AU  - Shiosaka, Sadao
AU  - Morikawa, Shota
TI  - Trophic modulation of gamma oscillations: The key role of processing protease for Neuregulin-1 and BDNF precursors
JF  - NEUROCHEMISTRY INTERNATIONAL
J2  - NEUROCHEM INT
VL  - 119
PY  - 2018
SP  - 2
EP  - 10
PG  - 9
SN  - 0197-0186
DO  - 10.1016/j.neuint.2017.12.002
UR  - https://m2.mtmt.hu/api/publication/30585473
ID  - 30585473
AB  - Gamma oscillations within the cerebral cortex and hippocampus are associated with cognitive processes, including attention, sensory perception, and memory formation; a deficit in gamma regulation is a common symptom of neurologic and psychiatric disorders. Accumulating evidence has suggested that gamma oscillations result from the synchronized activity of cell assemblies coordinated mainly by parvalbumin-positive inhibitory interneurons. The modulator molecules for pan/albumin-positive interneurons are major research targets and have the potential to control the specific oscillatory rhythm and behavior originating from neural coordination. Neuregulin-1 and brain-derived neurotrophic factor have been focused on as synaptic trophic factors that are associated with gamma oscillations. Synaptic activity converts precursor trophic factors into their biologically active forms by proteolytic cleavage, which could, in turn, modulate cell excitability and synaptic plasticity through each receptor's signaling. From these findings, the processing of trophic factors by proteases in a synaptic microenvironment might involve gamma oscillations during cognition. Here, we review the trophic modulation of gamma oscillations through extracellular proteolysis and its implications in neuronal diseases. (C) 2017 Elsevier Ltd. All rights reserved.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Bikbaev, Arthur
AU  - Manahan-Vaughan, Denise
TI  - Metabotropic glutamate receptor, mGlu5, regulates hippocampal synaptic plasticity and is required for tetanisation-triggered changes in theta and gamma oscillations
JF  - NEUROPHARMACOLOGY
J2  - NEUROPHARMACOLOGY
VL  - 115
PY  - 2017
SP  - 20
EP  - 29
PG  - 10
SN  - 0028-3908
DO  - 10.1016/j.neuropharm.2016.06.004
UR  - https://m2.mtmt.hu/api/publication/27029821
ID  - 27029821
LA  - English
DB  - MTMT
ER  - 

TY  - CHAP
AU  - Hagena, Hardy
AU  - Manahan-Vaughan, Denise
ED  - Ngomba, R
ED  - Di Giovanni, G
ED  - Battaglia, G
ED  - Nicoletti, F
TI  - mGlu5: A Metabotropic Glutamate Receptor at the Hub of Hippocampal Information Processing, Persistent Synaptic Plasticity, and Long-Term Memory
T2  - mGLU Receptors.
PB  - Humana Press
CY  - Cham
SN  - 9783319561707
T3  - The Receptors, ISSN 1048-6909 ; 31.
PY  - 2017
SP  - 79
EP  - 101
PG  - 23
DO  - 10.1007/978-3-319-56170-7_5
UR  - https://m2.mtmt.hu/api/publication/31840159
ID  - 31840159
AB  - In the hippocampus, the metabotropic glutamate (mGlu) receptor, mGlu5, plays a very prominent role in synaptic information storage and memory. This receptor enables persistent (>24 h) forms of synaptic plasticity, in the form of long-term potentiation (LTP) and long-term depression (LTD), and is also required for plasticity forms that are directly modulated by spatial learning. mGlu5 supports hippocampal neuronal oscillations that occur during synaptic plasticity events, supports the stabilization of place fields, and regulates the direction of change in synaptic weights in specific synaptic subcompartments of the hippocampus. Furthermore, dysfunctions in this receptor are associated with potent disturbances of hippocampus-dependent cognition. We propose that the mGlu5 receptor lies at the hub of hippocampal information processing and is pivotal to the accurate, long-term, and reliable acquisition and encoding of new spatial experiences and cognitive representations.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Kalweit, Alexander N
AU  - Amanpour-Gharaei, Bezhad
AU  - Colitti-Klausnitzer, Jens
AU  - Manahan-Vaughan, Denise
TI  - Changes in Neuronal Oscillations Accompany the Loss of Hippocampal LTP that Occurs in an Animal Model of Psychosis
JF  - FRONTIERS IN BEHAVIORAL NEUROSCIENCE
J2  - FRONT BEHAV NEUROSCI
VL  - 11
PY  - 2017
PG  - 15
SN  - 1662-5153
DO  - 10.3389/fnbeh.2017.00036
UR  - https://m2.mtmt.hu/api/publication/26565341
ID  - 26565341
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Olajos, Gábor
AU  - Bartus, Éva
AU  - Schuster, Ildikó
AU  - Lautner, Gergely
AU  - Gyurcsányi, Ervin Róbert
AU  - Szögi, Titanilla
AU  - Fülöp, Lívia
AU  - Martinek, Tamás
TI  - Multivalent foldamer-based affinity assay for selective recognition of Aβ oligomers
JF  - ANALYTICA CHIMICA ACTA
J2  - ANAL CHIM ACTA
VL  - 960
PY  - 2017
SP  - 131
EP  - 137
PG  - 7
SN  - 0003-2670
DO  - 10.1016/j.aca.2017.01.013
UR  - https://m2.mtmt.hu/api/publication/3193785
ID  - 3193785
N1  - Megjegyzés-26494651
N1 Funding details: TÁMOP-4.2.4.A/2-11/1-2012-0001, ESF, European Social Fund
N1 Funding text: This work was supported by the Hungarian Academy of Sciences, Lendület programs (LP-2011-009 and LP2013-63), Gedeon Richter Plc. (TP7-017), the Hungarian Research Foundation (OTKA K112442) and Gedeon Richter's Talentum Foundation (Ph.D. Scholarship to É.B.). This research received financing also from the European Union and the State of Hungary, co-financed by the European Social Fund in the framework of TÁMOP-4.2.4.A/2-11/1-2012-0001 ‘National Excellence Program’. This work was supported by the Hungarian Brain Research Program - Grant No. KTIA_13_NAP-A-III/7.
Funding Agency and Grant Number: Hungarian Academy of Sciences, Lendulet program [LP-2011-009, LP2013-63]; Gedeon Richter Plc. [TP7-017]; Hungarian Research Foundation [OTKA K112442]; Gedeon Richter's Talentum Foundation; European Union; State of Hungary; European Social Fund 'National Excellence Program' [TAMOP-4.2.4.A/2-11/1-2012-0001]; Hungarian Brain Research Program [KTIA_13_-NAP-A-III/7]\n Funding text: This work was supported by the Hungarian Academy of Sciences, Lendulet programs (LP-2011-009 and LP2013-63), Gedeon Richter Plc. (TP7-017), the Hungarian Research Foundation (OTKA K112442) and Gedeon Richter's Talentum Foundation (Ph.D. Scholarship to E.B.). This research received financing also from the European Union and the State of Hungary, co-financed by the European Social Fund in the framework of TAMOP-4.2.4.A/2-11/1-2012-0001 'National Excellence Program'. This work was supported by the Hungarian Brain Research Program - Grant No. KTIA_13_-NAP-A-III/7.\n
Funding Agency and Grant Number: Hungarian Academy of Sciences, Lendulet program [LP-2011-009, LP2013-63]; Gedeon Richter Plc. [TP7-017]; Hungarian Research Foundation [OTKA K112442]; Gedeon Richter's Talentum Foundation; European Union; State of Hungary; European Social Fund 'National Excellence Program' [TAMOP-4.2.4.A/2-11/1-2012-0001]; Hungarian Brain Research Program [KTIA_13_-NAP-A-III/7]
            Funding text: This work was supported by the Hungarian Academy of Sciences, Lendulet programs (LP-2011-009 and LP2013-63), Gedeon Richter Plc. (TP7-017), the Hungarian Research Foundation (OTKA K112442) and Gedeon Richter's Talentum Foundation (Ph.D. Scholarship to E.B.). This research received financing also from the European Union and the State of Hungary, co-financed by the European Social Fund in the framework of TAMOP-4.2.4.A/2-11/1-2012-0001 'National Excellence Program'. This work was supported by the Hungarian Brain Research Program - Grant No. KTIA_13_-NAP-A-III/7.
Institute of Pharmaceutical Analysis, University of Szeged, Somogyi u. 4, Szeged, 6720, Hungary            
            Department of Medical Chemistry, University of Szeged, Dóm tér 8, Szeged, 6720, Hungary            
            MTA-BME Lendület Chemical Nanosensors Research Group, Department of Inorganic and Analytical Chemistry, Budapest University of Technology and Economics, Szt. Gellért tér 4, Budapest, 1111, Hungary            
            Cited By :2            
            Export Date: 24 September 2019            
            CODEN: ACACA            
            Correspondence Address: Fülöp, L.; Department of Medical Chemistry, University of Szeged, Dóm tér 8, Hungary; email: fulop.livia@med.u-szeged.hu            
            Chemicals/CAS: amyloid beta protein, 109770-29-8; Amyloid beta-Peptides; Protein Aggregates            
            Funding details: Richter Gedeon Talentum Alapítvány            
            Funding details: European Social Fund, ESF, A/2-11/1-2012-0001            
            Funding details: Magyar Tudományos Akadémia, MTA, LP2013-63, LP-2011-009            
            Funding details: Gedeon Richter, TP7-017            
            Funding details: K112442            
            Funding details: KTIA_13_NAP-A-III/7            
            Funding text 1: This work was supported by the Hungarian Academy of Sciences, Lend?let programs (LP-2011-009 and LP2013-63), Gedeon Richter Plc. (TP7-017), the Hungarian Research Foundation (OTKA K112442) and Gedeon Richter's Talentum Foundation (Ph.D. Scholarship to ?.B.). This research received financing also from the European Union and the State of Hungary, co-financed by the European Social Fund in the framework of T?MOP-4.2.4.A/2-11/1-2012-0001 ?National Excellence Program?. This work was supported by the Hungarian Brain Research Program - Grant No. KTIA_13_NAP-A-III/7.
CAplus AN 2017:198655; MEDLINE PMID: 28193356 (Journal; Article);
AB  - Abstract Mimicking the molecular recognition functionality of antibodies is a great challenge. Foldamers are attractive candidates because of their relatively small size and designable interaction surface. This paper describes a sandwich type enzyme-linked immunoassay with a tetravalent β-peptide foldamer helix array as capture element and enzyme labeled tracer antibodies. The assay was found to be selective to β-amyloid oligomeric species with surface features transiently present in ongoing aggregation. In optimized conditions, with special emphasis on the foldamer immobilization, a detection limit of 5 pM was achieved with a linear range of 10–500 pM. These results suggest that protein mimetic foldamers can be useful tools in biosensors and affinity assays.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Sanchez-Rodriguez, Irene
AU  - Temprano-Carazo, Sara
AU  - Najera, Alberto
AU  - Djebari, Souhail
AU  - Yajeya, Javier
AU  - Gruart, Agnes
AU  - Delgado-Garcia, Jose M
AU  - Jimenez-Diaz, Lydia
AU  - Navarro-Lopez, Juan D
TI  - Activation of G-protein-gated inwardly rectifying potassium (Kir3/GirK) channels rescues hippocampal functions in a mouse model of early amyloid-β pathology
JF  - SCIENTIFIC REPORTS
J2  - SCI REP
VL  - 7
PY  - 2017
PG  - 13
SN  - 2045-2322
DO  - 10.1038/s41598-017-15306-8
UR  - https://m2.mtmt.hu/api/publication/27147147
ID  - 27147147
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - More, Sandeep Vasant
AU  - Kumar, Hemant
AU  - Cho, Duk-Yeon
AU  - Yun, Yo-Sep
AU  - Choi, Dong-Kug
TI  - Toxin-Induced Experimental Models of Learning and Memory Impairment
JF  - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
J2  - INT J MOL SCI
VL  - 17
PY  - 2016
IS  - 9
PG  - 34
SN  - 1661-6596
DO  - 10.3390/ijms17091447
UR  - https://m2.mtmt.hu/api/publication/26224480
ID  - 26224480
LA  - English
DB  - MTMT
ER  -