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		<title>BMC Neuroscience - Most viewed articles</title>
		<link>http://www.biomedcentral.com/bmcneurosci/mostviewed/</link>
		<description>Most viewed articles in last 30 days from BMC Neuroscience (ISSN 1471-2202) published by 
				
				BioMed Central
		</description>
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				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2202/9/48"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2202/9/56"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2202/9/61"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2202/9/58"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2202/9/60"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2202/9/62"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2202/5/42"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2202/9/66"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2202/9/59"/>			    
            
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		<item rdf:about="http://www.biomedcentral.com/1471-2202/9/48">
            
            <title>Unforgettable film music: The role of emotion in episodic long-term memory for music</title>
			<description>Background:
Specific pieces of music can elicit strong emotions in listeners and, possibly in connection with these emotions, can be remembered even years later. However, episodic memory for emotional music compared with less emotional music has not yet been examined. We investigated whether emotional music is remembered better than less emotional music. Also, we examined the influence of musical structure on memory performance.
Results:
Recognition of 40 musical excerpts was investigated as a function of arousal, valence, and emotional intensity ratings of the music. In the first session the participants judged valence and arousal of the musical pieces. One week later, participants listened to the 40 old and 40 new musical excerpts randomly interspersed and were asked to make an old/new decision as well as to indicate arousal and valence of the pieces. Musical pieces that were rated as very positive were recognized significantly better.
Conclusion:
Musical excerpts rated as very positive are remembered better. Valence seems to be an important modulator of episodic long-term memory for music. Evidently, strong emotions related to the musical experience facilitate memory formation and retrieval.</description>
			<link>http://www.biomedcentral.com/1471-2202/9/48</link>		
			<dc:creator>Susann Eschrich, Thomas F M&#252;nte and Eckart O Altenm&#252;ller</dc:creator>
			<dc:source>BMC Neuroscience 2008, 9:48</dc:source>
			<dc:subject>Number of accesses: 461</dc:subject>
			<dc:date>2008-05-28</dc:date>
			<dc:identifier>doi:10.1186/1471-2202-9-48</dc:identifier>
			
			
							
					<prism:publicationName>BMC Neuroscience</prism:publicationName>
					
			
							
					<prism:issn>1471-2202</prism:issn>
					
			
							
					<prism:volume>9</prism:volume>
					
			
							
					<prism:startingPage>48</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-05-28</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-2202/9/56">
            
            <title>Neural markers of a greater female responsiveness to social stimuli</title>
			<description>Background:
There is fMRI evidence that women are neurally predisposed to process infant laughter and crying. Other findings show that women might be more empathic and sensitive than men to emotional facial expressions. However, no gender difference in the brain responses to persons and unanimated scenes has hitherto been demonstrated.
Results:
Twenty-four men and women viewed 220 images portraying persons or landscapes and ERPs were recorded from 128 sites. In women, but not in men, the N2 component (210&#8211;270) was much larger to persons than to scenes. swLORETA showed significant bilateral activation of FG (BA19/37) in both genders when viewing persons as opposed to scenes. Only women showed a source of activity in the STG and in the right MOG (extra-striate body area, EBA), and only men in the left parahippocampal area (PPA).
Conclusion:
A significant gender difference was found in activation of the left and right STG (BA22) and the cingulate cortex for the subtractive condition women minus men, thus indicating that women might have a greater preference or interest for social stimuli (faces and persons).</description>
			<link>http://www.biomedcentral.com/1471-2202/9/56</link>		
			<dc:creator>Alice M Proverbio, Alberto Zani and Roberta Adorni</dc:creator>
			<dc:source>BMC Neuroscience 2008, 9:56</dc:source>
			<dc:subject>Number of accesses: 460</dc:subject>
			<dc:date>2008-06-30</dc:date>
			<dc:identifier>doi:10.1186/1471-2202-9-56</dc:identifier>
			
			
							
					<prism:publicationName>BMC Neuroscience</prism:publicationName>
					
			
							
					<prism:issn>1471-2202</prism:issn>
					
			
							
					<prism:volume>9</prism:volume>
					
			
							
					<prism:startingPage>56</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-06-30</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-2202/9/61">
            
            <title>Time-dependent biphasic modulation of human BDNF by antidepressants in neuroblastoma cells</title>
			<description>Background:
Recent rodent studies reported that antidepressant treatments affect the expression of brain-derived neurotrophic factor (BDNF) mRNA in a way that is dependent on treatment duration, by selective modulation of different BDNF transcripts. However, no data are available for the human BDNF gene. We studied the effect of different antidepressants on BDNF mRNA expression in human neuroblastoma SH-SY5Y cells.
Results:
Cultured cells were treated with the antidepressants fluoxetine, reboxetine and desipramine for different time lengths (6, 24, 48 hours). Expression of total BDNF mRNA was analyzed by reverse transcription PCR and levels of different BDNF transcripts were detected by hemi-nested PCR with specific primers.Short-term treatment (6 hours) with reboxetine or desipramine reduced total BDNF, whereas long-term treatment (48 hours) significantly increased total BDNF mRNA levels. These changes were accounted for by differential regulation of BDNF IV and VIa/b transcripts. Fluoxetine showed no significant effects.
Conclusion:
This is the first study showing biphasic changes in the expression of total and specific BDNF transcripts in human cells following antidepressant treatments. These findings suggest that biphasic induction of BDNF by antidepressants could be a feature common to rodents and humans and encourage the use of SH-SY5Y cells as a tool for investigation of drug effects on human genes.</description>
			<link>http://www.biomedcentral.com/1471-2202/9/61</link>		
			<dc:creator>Lorena Donnici, Ettore Tiraboschi, Daniela Tardito, Laura Musazzi, Giorgio Racagni and Maurizio Popoli</dc:creator>
			<dc:source>BMC Neuroscience 2008, 9:61</dc:source>
			<dc:subject>Number of accesses: 411</dc:subject>
			<dc:date>2008-07-05</dc:date>
			<dc:identifier>doi:10.1186/1471-2202-9-61</dc:identifier>
			
			
							
					<prism:publicationName>BMC Neuroscience</prism:publicationName>
					
			
							
					<prism:issn>1471-2202</prism:issn>
					
			
							
					<prism:volume>9</prism:volume>
					
			
							
					<prism:startingPage>61</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-07-05</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-2202/9/58">
            
            <title>Brain architecture in the terrestrial hermit crab Coenobita clypeatus (Anomura, Coenobitidae), a crustacean with a good aerial sense of smell</title>
			<description>Background:
During the evolutionary radiation of Crustacea, several lineages in this taxon convergently succeeded in meeting the physiological challenges connected to establishing a fully terrestrial life style. These physiological adaptations include the need for sensory organs of terrestrial species to function in air rather than in water. Previous behavioral and neuroethological studies have provided solid evidence that the land hermit crabs (Coenobitidae, Anomura) are a group of crustaceans that have evolved a good sense of aerial olfaction during the conquest of land. We wanted to study the central olfactory processing areas in the brains of these organisms and to that end analyzed the brain of Coenobita clypeatus (Herbst, 1791; Anomura, Coenobitidae), a fully terrestrial tropical hermit crab, by immunohistochemistry against synaptic proteins, serotonin, FMRFamide-related peptides, and glutamine synthetase.
Results:
The primary olfactory centers in this species dominate the brain and are composed of many elongate olfactory glomeruli. The secondary olfactory centers that receive an input from olfactory projection neurons are almost equally large as the olfactory lobes and are organized into parallel neuropil lamellae. The architecture of the optic neuropils and those areas associated with antenna two suggest that C. clypeatus has visual and mechanosensory skills that are comparable to those of marine Crustacea.
Conclusion:
In parallel to previous behavioral findings of a good sense of aerial olfaction in C. clypeatus, our results indicate that in fact their central olfactory pathway is most prominent, indicating that olfaction is a major sensory modality that these brains process. Interestingly, the secondary olfactory neuropils of insects, the mushroom bodies, also display a layered structure (vertical and medial lobes), superficially similar to the lamellae in the secondary olfactory centers of C. clypeatus. More detailed analyses with additional markers will be necessary to explore the question if these similarities have evolved convergently with the establishment of superb aerial olfactory abilities or if this design goes back to a shared principle in the common ancestor of Crustacea and Hexapoda.</description>
			<link>http://www.biomedcentral.com/1471-2202/9/58</link>		
			<dc:creator>Steffen Harzsch and Bill S Hansson</dc:creator>
			<dc:source>BMC Neuroscience 2008, 9:58</dc:source>
			<dc:subject>Number of accesses: 404</dc:subject>
			<dc:date>2008-06-30</dc:date>
			<dc:identifier>doi:10.1186/1471-2202-9-58</dc:identifier>
			
			
							
					<prism:publicationName>BMC Neuroscience</prism:publicationName>
					
			
							
					<prism:issn>1471-2202</prism:issn>
					
			
							
					<prism:volume>9</prism:volume>
					
			
							
					<prism:startingPage>58</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-06-30</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-2202/9/60">
            
            <title>Synchrony between orientation-selective neurons is modulated during adaptation-induced plasticity in cat visual cortex</title>
			<description>Background:
Visual neurons respond essentially to luminance variations occurring within their receptive fields. In primary visual cortex, each neuron is a filter for stimulus features such as orientation, motion direction and velocity, with the appropriate combination of features eliciting maximal firing rate. Temporal correlation of spike trains was proposed as a potential code for linking the neuronal responses evoked by various features of a same object. In the present study, synchrony strength was measured between cells following an adaptation protocol (prolonged exposure to a non-preferred stimulus) which induce plasticity of neurons' orientation preference.
Results:
Multi-unit activity from area 17 of anesthetized adult cats was recorded. Single cells were sorted out and (1) orientation tuning curves were measured before and following 12 min adaptation and 60 min after adaptation (2) pairwise synchrony was measured by an index that was normalized in relation to the cells' firing rate. We first observed that the prolonged presentation of a non-preferred stimulus produces attractive (58%) and repulsive (42%) shifts of cell's tuning curves. It follows that the adaptation-induced plasticity leads to changes in preferred orientation difference, i.e. increase or decrease in tuning properties between neurons. We report here that, after adaptation, the neuron pairs that shared closer tuning properties display a significant increase of synchronization. Recovery from adaptation was accompanied by a return to the initial synchrony level.
Conclusion:
We conclude that synchrony reflects the similarity in neurons' response properties, and varies accordingly when these properties change.</description>
			<link>http://www.biomedcentral.com/1471-2202/9/60</link>		
			<dc:creator>Narcis Ghisovan, Abdellatif Nemri, Svetlana Shumikhina and Stephane Molotchnikoff</dc:creator>
			<dc:source>BMC Neuroscience 2008, 9:60</dc:source>
			<dc:subject>Number of accesses: 393</dc:subject>
			<dc:date>2008-07-03</dc:date>
			<dc:identifier>doi:10.1186/1471-2202-9-60</dc:identifier>
			
			
							
					<prism:publicationName>BMC Neuroscience</prism:publicationName>
					
			
							
					<prism:issn>1471-2202</prism:issn>
					
			
							
					<prism:volume>9</prism:volume>
					
			
							
					<prism:startingPage>60</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-07-03</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-2202/9/62">
            
            <title>NF-kappaB activation is associated with homocysteine-induced injury in Neuro2a cells</title>
			<description>Background:
Perinatal exposure to hyperhomocysteinemia might disturb neurogenesis during brain development and growth. Also, high levels of homocysteine trigger neurodegeneration in several experimental models. However, the putative mechanisms of homocysteine-induced toxicity in the developing nervous system have poorly been elucidated. This study was aimed to investigate homocysteine effects in undifferentiated neuroblastoma cells, Neuro2a.
Results:
A 4 h exposure to homocysteine in a concentration range of 10&#8211;100 &#956;M did not affect cell viability and ROS production in Neuro2a cell cultures. Instead, ROS levels were increased by two-three folds in cells treated with 250 &#956;M and 500 &#956;M homocysteine, respectively, in comparison with control cells. Also, the highest homocysteine dose significantly reduced the viable cell number by 40%. Notably, the treatment with homocysteine (250 &#956;M&#8211;500 &#956;M) in the presence of antioxidants, such as N-acetylcysteine and IRFI 016, a synthetic &#945;-tocopherol analogue, recovered cell viability and significantly reduced homocysteine-evoked increases in ROS production. Moreover, antioxidants, particularly IRFI 016, were able to counteract NF-&#954;B activation induced by 250 &#956;M homocysteine.Cell treatment with 250 &#956;M homocysteine also triggered the onset of apoptosis, as demonstrated by the increased expression of early apoptotic markers such as Bax, caspase-3 and p53. In contrast, Bcl2 expression was not affected by homocysteine exposure. Interestingly, the specific inhibition of NF-&#954;B nuclear translocation by the synthetic peptide SN50 was able to almost completely suppress the homocysteine-evoked rises in pro-apoptotic protein expression as well as in caspase-3 activity. Further, also IRFI 016 and N-acetylcysteine were able to significantly reduce caspase-3 activation induced by homocysteine treatment.
Conclusion:
These observations suggest an involvement of redox state alterations and activated NF-&#954;B in apoptosis onset triggered by homocysteine in neuroblastoma cells Neuro2a. However, further investigations are needed to characterize molecular events involved in the NF-&#954;B activation induced by homocysteine.</description>
			<link>http://www.biomedcentral.com/1471-2202/9/62</link>		
			<dc:creator>Nadia Ferlazzo, Salvatore Condello, Monica Curr&#242;, Giulia Parisi, Riccardo Ientile and Daniela Caccamo</dc:creator>
			<dc:source>BMC Neuroscience 2008, 9:62</dc:source>
			<dc:subject>Number of accesses: 377</dc:subject>
			<dc:date>2008-07-07</dc:date>
			<dc:identifier>doi:10.1186/1471-2202-9-62</dc:identifier>
			
			
							
					<prism:publicationName>BMC Neuroscience</prism:publicationName>
					
			
							
					<prism:issn>1471-2202</prism:issn>
					
			
							
					<prism:volume>9</prism:volume>
					
			
							
					<prism:startingPage>62</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-07-07</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-2202/5/42">
            
            <title>An information integration theory of consciousness</title>
			<description>Background:
Consciousness poses two main problems. The first is understanding the conditions that determine to what extent a system has conscious experience. For instance, why is our consciousness generated by certain parts of our brain, such as the thalamocortical system, and not by other parts, such as the cerebellum? And why are we conscious during wakefulness and much less so during dreamless sleep? The second problem is understanding the conditions that determine what kind of consciousness a system has. For example, why do specific parts of the brain contribute specific qualities to our conscious experience, such as vision and audition?Presentation of the hypothesisThis paper presents a theory about what consciousness is and how it can be measured. According to the theory, consciousness corresponds to the capacity of a system to integrate information. This claim is motivated by two key phenomenological properties of consciousness: differentiation &#8211; the availability of a very large number of conscious experiences; and integration &#8211; the unity of each such experience. The theory states that the quantity of consciousness available to a system can be measured as the &#934; value of a complex of elements. &#934; is the amount of causally effective information that can be integrated across the informational weakest link of a subset of elements. A complex is a subset of elements with &#934;>0 that is not part of a subset of higher &#934;. The theory also claims that the quality of consciousness is determined by the informational relationships among the elements of a complex, which are specified by the values of effective information among them. Finally, each particular conscious experience is specified by the value, at any given time, of the variables mediating informational interactions among the elements of a complex.Testing the hypothesisThe information integration theory accounts, in a principled manner, for several neurobiological observations concerning consciousness. As shown here, these include the association of consciousness with certain neural systems rather than with others; the fact that neural processes underlying consciousness can influence or be influenced by neural processes that remain unconscious; the reduction of consciousness during dreamless sleep and generalized seizures; and the time requirements on neural interactions that support consciousness.Implications of the hypothesisThe theory entails that consciousness is a fundamental quantity, that it is graded, that it is present in infants and animals, and that it should be possible to build conscious artifacts.</description>
			<link>http://www.biomedcentral.com/1471-2202/5/42</link>		
			<dc:creator>Giulio Tononi</dc:creator>
			<dc:source>BMC Neuroscience 2004, 5:42</dc:source>
			<dc:subject>Number of accesses: 342</dc:subject>
			<dc:date>2004-11-02</dc:date>
			<dc:identifier>doi:10.1186/1471-2202-5-42</dc:identifier>
			
			
							
					<prism:publicationName>BMC Neuroscience</prism:publicationName>
					
			
							
					<prism:issn>1471-2202</prism:issn>
					
			
							
					<prism:volume>5</prism:volume>
					
			
							
					<prism:startingPage>42</prism:startingPage>
					
			
							
					<prism:publicationDate>2004-11-02</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-2202/9/66">
            
            <title>Identification of a set of genes showing regionally enriched expression in the mouse brain</title>
			<description>Background:
The Pleiades Promoter Project aims to improve gene therapy by designing human mini-promoters (&lt; 4 kb) that drive gene expression in specific brain regions or cell-types of therapeutic interest. Our goal was to first identify genes displaying regionally enriched expression in the mouse brain so that promoters designed from orthologous human genes can then be tested to drive reporter expression in a similar pattern in the mouse brain.
Results:
We have utilized LongSAGE to identify regionally enriched transcripts in the adult mouse brain. As supplemental strategies, we also performed a meta-analysis of published literature and inspected the Allen Brain Atlas in situ hybridization data. From a set of approximately 30,000 mouse genes, 237 were identified as showing specific or enriched expression in 30 target regions of the mouse brain. GO term over-representation among these genes revealed co-involvement in various aspects of central nervous system development and physiology.
Conclusion:
Using a multi-faceted expression validation approach, we have identified mouse genes whose human orthologs are good candidates for design of mini-promoters. These mouse genes represent molecular markers in several discrete brain regions/cell-types, which could potentially provide a mechanistic explanation of unique functions performed by each region. This set of markers may also serve as a resource for further studies of gene regulatory elements influencing brain expression.</description>
			<link>http://www.biomedcentral.com/1471-2202/9/66</link>		
			<dc:creator>Cletus A D'Souza, Vikramjit Chopra, Richard Varhol, Yuan-Yun Xie, Slavita Bohacec, Yongjun Zhao, Lisa LC Lee, Mikhail Bilenky, Elodie Portales-Casamar, An He, Wyeth W Wasserman, Daniel Goldowitz, Marco A Marra, Robert A Holt, Elizabeth M Simpson and Steven JM Jones</dc:creator>
			<dc:source>BMC Neuroscience 2008, 9:66</dc:source>
			<dc:subject>Number of accesses: 337</dc:subject>
			<dc:date>2008-07-14</dc:date>
			<dc:identifier>doi:10.1186/1471-2202-9-66</dc:identifier>
			
			
							
					<prism:publicationName>BMC Neuroscience</prism:publicationName>
					
			
							
					<prism:issn>1471-2202</prism:issn>
					
			
							
					<prism:volume>9</prism:volume>
					
			
							
					<prism:startingPage>66</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-07-14</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-2202/9/59">
            
            <title>Sub region-specific modulation of synchronous neuronal burst firing after a kainic acid insult in organotypic hippocampal cultures</title>
			<description>Background:
Excitotoxicity occurs in a number of pathogenic states including stroke and epilepsy. The adaptations of neuronal circuits in response to such insults may be expected to play an underlying role in pathogenesis. Synchronous neuronal firing can be induced in isolated hippocampal slices and involves all regions of this structure, thereby providing a measure of circuit activity. The effect of an excitotoxic insult (kainic acid, KA) on Mg2+-free-induced synchronized neuronal firing was tested in organotypic hippocampal culture by measuring extracellular field activity in CA1 and CA3.
Results:
Within 24 hrs of the insult regional specific changes in neuronal firing patterns were evident as: (i) a dramatic reduction in the ability of CA3 to generate firing; and (ii) a contrasting increase in the frequency and duration of synchronized neuronal firing events in CA1. Two distinct processes underlie the increased propensity of CA1 to generate synchronized burst firing; a lack of ability of the CA3 region to 'pace' CA1 resulting in an increased frequency of synchronized events; and a change in the 'intrinsic' properties limited to the CA1 region, which is responsible for increased event duration. Neuronal quantification using NeuN immunoflurescent staining and stereological confocal microscopy revealed no significant cell loss in hippocampal sub regions, suggesting that changes in the properties of neurons within this region were responsible for the KA-mediated excitability changes.
Conclusion:
These results provide novel insight into adaptation of hippocampal circuits following excitotoxic injury. KA-mediated disruption of the interplay between CA3 and CA1 clearly increases the propensity to synchronized firing in CA1.</description>
			<link>http://www.biomedcentral.com/1471-2202/9/59</link>		
			<dc:creator>Christopher A Reid, Brendan EL Adams, Damian Myers, Terence J O'Brien and David A Williams</dc:creator>
			<dc:source>BMC Neuroscience 2008, 9:59</dc:source>
			<dc:subject>Number of accesses: 330</dc:subject>
			<dc:date>2008-07-02</dc:date>
			<dc:identifier>doi:10.1186/1471-2202-9-59</dc:identifier>
			
			
							
					<prism:publicationName>BMC Neuroscience</prism:publicationName>
					
			
							
					<prism:issn>1471-2202</prism:issn>
					
			
							
					<prism:volume>9</prism:volume>
					
			
							
					<prism:startingPage>59</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-07-02</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1471-2202/9/22">
            
            <title>Peripheral injection of human umbilical cord blood stimulates neurogenesis in the aged rat brain</title>
			<description>Background:
Neurogenesis continues to occur throughout life but dramatically decreases with increasing age. This decrease is mostly related to a decline in proliferative activity as a result of an impoverishment of the microenvironment of the aged brain, including a reduction in trophic factors and increased inflammation.
Results:
We determined that human umbilical cord blood mononuclear cells (UCBMC) given peripherally, by an intravenous injection, could rejuvenate the proliferative activity of the aged neural stem/progenitor cells. This increase in proliferation lasted for at least 15 days after the delivery of the UCBMC. Along with the increase in proliferation following UCBMC treatment, an increase in neurogenesis was also found in the aged animals. The increase in neurogenesis as a result of UCBMC treatment seemed to be due to a decrease in inflammation, as a decrease in the number of activated microglia was found and this decrease correlated with the increase in neurogenesis.
Conclusion:
The results demonstrate that a single intravenous injection of UCBMC in aged rats can significantly improve the microenvironment of the aged hippocampus and rejuvenate the aged neural stem/progenitor cells. Our results raise the possibility of a peripherally administered cell therapy as an effective approach to improve the microenvironment of the aged brain.</description>
			<link>http://www.biomedcentral.com/1471-2202/9/22</link>		
			<dc:creator>Adam D Bachstetter, Mibel M Pabon, Michael J Cole, Charles E Hudson, Paul R Sanberg, Alison E Willing, Paula C Bickford and Carmelina Gemma</dc:creator>
			<dc:source>BMC Neuroscience 2008, 9:22</dc:source>
			<dc:subject>Number of accesses: 329</dc:subject>
			<dc:date>2008-02-14</dc:date>
			<dc:identifier>doi:10.1186/1471-2202-9-22</dc:identifier>
			
			
							
					<prism:publicationName>BMC Neuroscience</prism:publicationName>
					
			
							
					<prism:issn>1471-2202</prism:issn>
					
			
							
					<prism:volume>9</prism:volume>
					
			
							
					<prism:startingPage>22</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-02-14</prism:publicationDate>
					

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