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[PMID]: 25188513
[Au] Autor:Yazdankhah M; Farioli-Vecchioli S; Tonchev AB; Stoykova A; Cecconi F
[Ad] Address:1] IRCCS Fondazione Santa Lucia, Rome 00143, Italy [2] Department of Biology, University of Rome Tor Vergata, Rome 00133, Italy....
[Ti] Title:The autophagy regulators Ambra1 and Beclin 1 are required for adult neurogenesis in the brain subventricular zone.
[So] Source:Cell Death Dis;5:e1403, 2014.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Autophagy is a conserved proteolytic mechanism required for maintaining cellular homeostasis. The role of this process in vertebrate neural development is related to metabolic needs and stress responses, even though the importance of its progression has been observed in a number of circumstances, both in embryonic and in postnatal differentiating tissues. Here we show that the proautophagic proteins Ambra1 and Beclin 1, involved in the initial steps of autophagosome formation, are highly expressed in the adult subventricular zone (SVZ), whereas their downregulation in adult neural stem cells in vitro leads to a decrease in cell proliferation, an increase in basal apoptosis and an augmented sensitivity to DNA-damage-induced death. Further, Beclin 1 heterozygosis in vivo results in a significant reduction of proliferating cells and immature neurons in the SVZ, accompanied by a marked increase in apoptotic cell death. In sum, we propose that Ambra1- and Beclin 1-mediated autophagy plays a crucial role in adult neurogenesis, by controlling the survival of neural precursor cells.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1409
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1038/cddis.2014.358

  2 / 1237436 MEDLINE  
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[PMID]: 25165877
[Au] Autor:Milosch N; Tanriöver G; Kundu A; Rami A; François JC; Baumkötter F; Weyer SW; Samanta A; Jäschke A; Brod F; Buchholz CJ; Kins S; Behl C; Müller UC; Kögel D
[Ad] Address:Experimental Neurosurgery, Goethe University Hospital, Frankfurt am Main, Germany....
[Ti] Title:Holo-APP and G-protein-mediated signaling are required for sAPPα-induced activation of the Akt survival pathway.
[So] Source:Cell Death Dis;5:e1391, 2014.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Accumulating evidence indicates that loss of physiologic amyloid precursor protein (APP) function leads to reduced neuronal plasticity, diminished synaptic signaling and enhanced susceptibility of neurons to cellular stress during brain aging. Here we investigated the neuroprotective function of the soluble APP ectodomain sAPPα (soluble APPα), which is generated by cleavage of APP by α-secretase along the non-amyloidogenic pathway. Recombinant sAPPα protected primary hippocampal neurons and SH-SY5Y neuroblastoma cells from cell death induced by trophic factor deprivation. We show that this protective effect is abrogated in neurons from APP-knockout animals and APP-depleted SH-SY5Y cells, but not in APP-like protein 1- and 2- (APLP1 and APLP2) depleted cells, indicating that expression of membrane-bound holo-APP is required for sAPPα-dependent neuroprotection. Trophic factor deprivation diminished the activity of the Akt survival pathway. Strikingly, both recombinant sAPPα and the APP-E1 domain were able to stimulate Akt activity in wild-type (wt) fibroblasts, SH-SY5Y cells and neurons, but failed to rescue in APP-deficient neurons or fibroblasts. The ADAM10 (a disintegrin and metalloproteinase domain-containing protein 10) inhibitor GI254023X exacerbated neuron death in organotypic (hippocampal) slice cultures of wt mice subjected to trophic factor and glucose deprivation. This cell death-enhancing effect of GI254023X could be completely rescued by applying exogenous sAPPα. Interestingly, sAPPα-dependent Akt induction was unaffected in neurons of APP-ΔCT15 mice that lack the C-terminal YENPTY motif of the APP intracellular region. In contrast, sAPPα-dependent rescue of Akt activation was completely abolished in APP mutant cells lacking the G-protein interaction motif located in the APP C-terminus and by blocking G-protein-dependent signaling with pertussis toxin. Collectively, our data provide new mechanistic insights into the physiologic role of APP in antagonizing neurotoxic stress: they suggest that cell surface APP mediates sAPPα-induced neuroprotection via G-protein-coupled activation of the Akt pathway.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1038/cddis.2014.352

  3 / 1237436 MEDLINE  
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[PMID]: 25144721
[Au] Autor:Doeppner TR; Kaltwasser B; Teli MK; Bretschneider E; Bähr M; Hermann DM
[Ad] Address:Department of Neurology, University of Duisburg-Essen Medical School, Essen, Germany....
[Ti] Title:Effects of acute versus post-acute systemic delivery of neural progenitor cells on neurological recovery and brain remodeling after focal cerebral ischemia in mice.
[So] Source:Cell Death Dis;5:e1386, 2014.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Intravenous transplantation of neural progenitor cells (NPCs) induces functional recovery after stroke, albeit grafted cells are not integrated into residing neural networks. However, a systematic analysis of intravenous NPC delivery at acute and post-acute time points and their long-term consequences does not exist. Male C57BL6 mice were exposed to cerebral ischemia, and NPCs were intravenously grafted on day 0, on day 1 or on day 28. Animals were allowed to survive for up to 84 days. Mice and tissues were used for immunohistochemical analysis, flow cytometry, ELISA and behavioral tests. Density of grafted NPCs within the ischemic hemisphere was increased when cells were transplanted on day 28 as compared with transplantation on days 0 or 1. Likewise, transplantation on day 28 yielded enhanced neuronal differentiation rates of grafted cells. Post-ischemic brain injury, however, was only reduced when NPCs were grafted at acute time points. On the contrary, reduced post-ischemic functional deficits due to NPC delivery were independent of transplantation paradigms. NPC-induced neuroprotection after acute cell delivery was due to stabilization of the blood-brain barrier (BBB), reduction in microglial activation and modulation of both peripheral and central immune responses. On the other hand, post-acute NPC transplantation stimulated post-ischemic regeneration via enhanced angioneurogenesis and increased axonal plasticity. Acute NPC delivery yields long-term neuroprotection via enhanced BBB integrity and modulation of post-ischemic immune responses, whereas post-acute NPC delivery increases post-ischemic angioneurogenesis and axonal plasticity. Post-ischemic functional recovery, however, is independent of NPC delivery timing, which offers a broad therapeutic time window for stroke treatment.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1038/cddis.2014.359

  4 / 1237436 MEDLINE  
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[PMID]: 25144717
[Au] Autor:Tan MS; Tan L; Jiang T; Zhu XC; Wang HF; Jia CD; Yu JT
[Ad] Address:Department of Neurology, Qingdao Municipal Hospital, College of Medicine and Pharmaceutics, Ocean University of China, Qingdao, China....
[Ti] Title:Amyloid-ß induces NLRP1-dependent neuronal pyroptosis in models of Alzheimer's disease.
[So] Source:Cell Death Dis;5:e1382, 2014.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Increasing evidence has shown the aberrant expression of inflammasome-related proteins in Alzheimer's disease (AD) brain; these proteins, including NLRP1 inflammasome, are implicated in the execution of inflammatory response and pyroptotic death. Although current data are associated NLRP1 genetic variants with AD, the involvement of NLRP1 inflammasome in AD pathogenesis is still unknown. Using APPswe/PS1dE9 transgenic mice, we found that cerebral NLRP1 levels were upregulated. Our in vitro studies further showed that increased NLRP1-mediated caspase-1-dependent 'pyroptosis' in cultured cortical neurons in response to amyloid-ß. Moreover, we employed direct in vivo infusion of non-viral small-interfering RNA to knockdown NLRP1 or caspase-1 in APPswe/PS1dE9 brain, and discovered that these NLRP1 or caspase-1 deficiency mice resulted in significantly reduced neuronal pyroptosis and reversed cognitive impairments. Taken together, our findings indicate an important role for NLRP1/caspase-1 signaling in AD progression, and point to the modulation of NLRP1 inflammasome as a promising strategy for AD therapy.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1038/cddis.2014.348

  5 / 1237436 MEDLINE  
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[PMID]: 25132733
[Au] Autor:Santiago AR; Baptista FI; Santos PF; Cristóvão G; Ambrósio AF; Cunha RA; Gomes CA
[Ad] Address:Centre of Ophthalmology and Vision Sciences, IBILI, Faculty of Medicine, University of Coimbra, 3000-548 Coimbra, Portugal ; AIBILI, 3000-548 Coimbra, Portugal ; Center for Neuroscience and Cell Biology, Largo Marquês de Pombal, Universidade de Coimbra, 3004-517 Coimbra, Portugal ; Faculty of Medici...
[Ti] Title:Role of microglia adenosine A(2A) receptors in retinal and brain neurodegenerative diseases.
[So] Source:Mediators Inflamm;2014:465694, 2014.
[Is] ISSN:1466-1861
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Neuroinflammation mediated by microglial cells in the brain has been commonly associated with neurodegenerative diseases. Whether this microglia-mediated neuroinflammation is cause or consequence of neurodegeneration is still a matter of controversy. However, it is unequivocal that chronic neuroinflammation plays a role in disease progression and halting that process represents a potential therapeutic strategy. The neuromodulator adenosine emerges as a promising targeting candidate based on its ability to regulate microglial proliferation, chemotaxis, and reactivity through the activation of its G protein coupled A2A receptor (A2AR). This is in striking agreement with the ability of A2AR blockade to control several brain diseases. Retinal degenerative diseases have been also associated with microglia-mediated neuroinflammation, but the role of A2AR has been scarcely explored. This review aims to compare inflammatory features of Parkinson's and Alzheimer's diseases with glaucoma and diabetic retinopathy, discussing the therapeutic potential of A2AR in these degenerative conditions.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1155/2014/465694

  6 / 1237436 MEDLINE  
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[PMID]: 25118934
[Au] Autor:Li S; Deng J; Hou H; Tian J; Giunta B; Wang Y; Sawmiller D; Smith A; Sanberg PR; Obregon D; Mori T; Tan J
[Ad] Address:1] Rashid Laboratory for Developmental Neurobiology, Silver Child Development Center, Department of Psychiatry and Behavioral Neurosciences, Morsani College of Medicine, University of South Florida, Tampa, FL, USA [2] Center for Translational Research of Neurology Diseases, First Affiliated Hospital...
[Ti] Title:Specific antibody binding to the APP672-699 region shifts APP processing from α- to ß-cleavage.
[So] Source:Cell Death Dis;5:e1374, 2014.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Alzheimer's disease (AD), a progressive neurodegenerative disorder that is the most common cause of dementia in the elderly, is characterized by the accumulation of amyloid-ß (Aß) plaques and neurofibrillary tangles, as well as a progressive loss of synapses and neurons in the brain. The major pertinacious component of amyloid plaques is Aß, a variably sized peptide derived from the integral membrane protein amyloid precursor protein (APP). The Aß region of APP locates partly within its ecto- and trans-membrane domains. APP is cleaved by three proteases, designated as α-, ß-, and γ-secretases. Processing by ß- and γ-secretase cleaves the N- and C-terminal ends of the Aß region, respectively, releasing Aß, whereas α-secretase cleaves within the Aß sequence, releasing soluble APPα (sAPPα). The γ-secretase cleaves at several adjacent sites to yield Aß species containing 39-43 amino acid residues. Both α- and ß-cleavage sites of human wild-type APP are located in APP672-699 region (ectodomain of ß-C-terminal fragment, ED-ß-CTF or ED-C99). Therefore, the amino acid residues within or near this region are definitely pivotal for human wild-type APP function and processing. Here, we report that one ED-C99-specific monoclonal antibody (mAbED-C99) blocks human wild-type APP endocytosis and shifts its processing from α- to ß-cleavage, as evidenced by elevated accumulation of cell surface full-length APP and ß-CTF together with reduced sAPPα and α-CTF levels. Moreover, mAbED-C99 enhances the interactions of APP with cholesterol. Consistently, intracerebroventricular injection of mAbED-C99 to human wild-type APP transgenic mice markedly increases membrane-associated ß-CTF. All these findings suggest that APP672-699 region is critical for human wild-type APP processing and may provide new clues for the pathogenesis of sporadic AD.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1038/cddis.2014.336

  7 / 1237436 MEDLINE  
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[PMID]: 24998643
[Au] Autor:Pahor A; Jausovec N
[Ad] Address:University of Maribor, Slovenia.
[Ti] Title:The effects of theta transcranial alternating current stimulation (tACS) on fluid intelligence.
[So] Source:Int J Psychophysiol;93(3):322-31, 2014 Sep.
[Is] ISSN:1872-7697
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The objective of the study was to explore the influence of transcranial alternating current stimulation (tACS) on resting brain activity and on measures of fluid intelligence. Theta tACS was applied to the left parietal and left frontal brain areas of healthy participants after which resting electroencephalogram (EEG) data was recorded. Following sham/active stimulation, the participants solved two tests of fluid intelligence while their EEG was recorded. The results showed that active theta tACS affected spectral power in theta and alpha frequency bands. In addition, active theta tACS improved performance on tests of fluid intelligence. This influence was more pronounced in the group of participants that received stimulation to the left parietal area than in the group of participants that received stimulation to the left frontal area. Left parietal tACS increased performance on the difficult test items of both tests (RAPM and PF&C) whereas left frontal tACS increased performance only on the easy test items of one test (RAPM). The observed behavioral tACS influences were also accompanied by changes in neuroelectric activity. The behavioral and neuroelectric data tentatively support the P-FIT neurobiological model of intelligence.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Process

  8 / 1237436 MEDLINE  
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[PMID]: 24952215
[Au] Autor:Scolaro A; West R; Cohen AL
[Ad] Address:Central College, United States.
[Ti] Title:The ERP correlates of target checking are dependent upon the defining features of the prospective memory cues.
[So] Source:Int J Psychophysiol;93(3):298-304, 2014 Sep.
[Is] ISSN:1872-7697
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:In some contexts, prospective memory (PM) is thought to be dependent upon strategic monitoring of the environment for relevant cues. Behavioral data reveal that strategic monitoring is associated with slowing of response time for ongoing activity trials when a prospective component is added to the task, and functional imaging data reveal that monitoring is associated with recruitment of the anterior prefrontal cortex and other cortical structures. In the current study, event-related brain potentials (ERPs) were used to examine the neural correlates of target checking, one process underlying strategic monitoring. Consistent with previous research the behavioral data revealed a Stimulus Specific Interference Effect, wherein slowing of response time varied depending upon whether PM cues were words or nonwords. The ERP data also revealed that the neural correlates of target checking were sensitive to the defining features of the PM cues (i.e., were a word or nonword). When PM cues were words, the effect of target checking was associated with variation in ERP amplitude beginning around 100ms after stimulus onset. In contrast, when PM cues were nonwords, the effect of target checking on the ERPs did not emerge until around 200ms after stimulus onset. These data provide support for the multi-process view of PM by demonstrating that the pattern of neural recruitment related to target checking is sensitive to the defining characteristics of the PM cues.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Process

  9 / 1237436 MEDLINE  
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[PMID]: 24952214
[Au] Autor:Gudziol H; Fischer J; Bitter T; Guntinas-Lichius O
[Ad] Address:Department of Otorhinolaryngology, University Hospital Jena, Germany. Electronic address: Hilmar.gudziol@med.uni-jena.de....
[Ti] Title:Chemosensory event-related brain potentials (CSERP) after strictly monorhinal stimulation.
[So] Source:Int J Psychophysiol;93(3):305-10, 2014 Sep.
[Is] ISSN:1872-7697
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Using flow-olfactometer for chemosensory event related brain potentials (CSERP) the air escapes the contralateral nostril from the stimulated nostril via the nasopharynx. Theoretically, the escaping odorous airflow is able to stimulate the contralateral chemosensory receptors and might activate the olfactory or the trigeminal brain processes. Testing 18 healthy subjects, we were able to show that it was possible to generate CSERP by strictly monorhinal stimulation with closed contralateral nostril. That means that the rectangular shapes of the brief chemosensory stimuli were not disturbed. The latencies of N1 and P2 and the amplitudes (N1P2) of CSERP (stimulants: H2S and CO2) were not different with either open or closed contralateral nostril. The induced CSERP were independent of stimulated nostril side. Additionally we found that with closed contralateral nostril more than 90% of passive monorhinal chemosensory stimuli were perceived. In further imaging studies the presented paradigm should be applied with strictly monorhinal stimulation to investigate the chemosensory processing pathways with high time resolution (EEG/MEG).
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Process

  10 / 1237436 MEDLINE  
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[PMID]: 24905017
[Au] Autor:Hong X; Sun J; Bengson JJ; Tong S
[Ad] Address:School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200240, China; Center for Mind and Brain, University of California-Davis, Davis CA 95618, USA....
[Ti] Title:Age-related spatiotemporal reorganization during response inhibition.
[So] Source:Int J Psychophysiol;93(3):371-80, 2014 Sep.
[Is] ISSN:1872-7697
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:As a key high-level cognitive function in human beings, response inhibition is crucial for adaptive behavior. Previous neuroimaging studies have shown that older individuals exhibit greater neural activation than younger individuals during response inhibition tasks. This finding has been interpreted within a neural compensation framework, in which additional neural resources are recruited in response to age-related cognitive decline. Although this interpretation has received empirical support, the precise event-related temporal course of this age-related compensatory neural response remains unexplored. In the present study, we conducted source analysis on inhibition-related ERP components (i.e., N2 and P3) that were recorded while healthy younger and older adults participated in a visual Go/NoGo task. We found that older adults showed increased source current densities of the N2 and P3 components than younger adults, which support previous hemodynamic findings. Further, such age-related differences in neural activation were successfully separated between the N2 and P3 periods by source localization analysis. Interestingly, the increased activations in older adults were primarily localized to the right precentral and postcentral gyri during the N2 period, which shifted to the right dorsolateral prefrontal cortex and the right inferior frontal gyrus during the P3 period. Taken together, our results clearly illustrate the spatiotemporal dynamics of age-related functional brain reorganization, and further specify the exact temporal course at the millisecond scale by which age-related compensatory neural responses occur during response inhibition.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Process


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