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| 2. |
- Cooper-Kuhn, Christiana M, 1971, et al.
(author)
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Decreased neurogenesis after cholinergic forebrain lesion in the adult rat.
- 2004
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In: Journal of neuroscience research. - : Wiley. - 0360-4012 .- 1097-4547. ; 77:2, s. 155-65
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Journal article (peer-reviewed)abstract
- Adult neurogenesis has been shown to be regulated by a multitude of extracellular cues, including hormones, growth factors, and neurotransmitters. The cholinergic system of the basal forebrain is one of the key transmitter systems for learning and memory. Because adult neurogenesis has been implicated in cognitive performance, the present work aims at defining the role of cholinergic input for adult neurogenesis by using an immunotoxic lesion approach. The immunotoxin 192IgG-saporin was infused into the lateral ventricle of adult rats to selectively lesion cholinergic neurons of the cholinergic basal forebrain (CBF), which project to the two main regions of adult neurogenesis: the dentate gyrus and the olfactory bulb. Five weeks after lesioning, neurogenesis, defined by the number of cells colocalized for bromodeoxyuridine (BrdU) and the neuronal nuclei marker NeuN, declined significantly in the granule cell layers of the dentate gyrus and olfactory bulb. Furthermore, immunotoxic lesions to the CBF led to increased numbers of apoptotic cells specifically in the subgranular zone, the progenitor region of the dentate gyrus, and within the periglomerular layer of the olfactory bulb. We propose that the cholinergic system plays a survival-promoting role for neuronal progenitors and immature neurons within regions of adult neurogenesis, similar to effects observed previously during brain development. As a working hypothesis, neuronal loss within the CBF system leads not only to cognitive deficits but may also alter on a cellular level the functionality of the dentate gyrus, which in turn may aggravate cognitive deficits.
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| 3. |
- Kuhn, Hans-Georg, 1961, et al.
(author)
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Bromodeoxyuridine and the detection of neurogenesis.
- 2007
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In: Current pharmaceutical biotechnology. - 1873-4316. ; 8:3, s. 127-31
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Research review (peer-reviewed)abstract
- Bromodeoxyuridine (BrdU) is widely used for labeling dividing cells to determine their fate. In particular, the analysis of neurogenesis in the adult mammalian brain has made significant progress through the use of this technique. However; when using BrdU for labeling, there are several issues to consider in order to minimalize possible cytotoxicity or false-positive labeling. This current review summarizes methodological and technical aspects of BrdU administration and detection, compares alternative methods and gives recommendations on how to avoid labeling artifacts.
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| 4. |
- Kuhn, Hans-Georg, 1961, et al.
(author)
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Changes in neurogenesis in dementia and Alzheimer mouse models: are they functionally relevant?
- 2007
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In: European archives of psychiatry and clinical neuroscience. - : Springer Science and Business Media LLC. - 0940-1334 .- 1433-8491. ; 257:5, s. 281-9
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Research review (peer-reviewed)abstract
- Alzheimer's disease and related dementias are devastating disorders that lead to the progressive decline of cognitive functions. Characteristic features are severe brain atrophy, paralleled by accumulation of beta amyloid and neurofibrillary tangles. With the discovery of neurogenesis in the adult brain, the hopes have risen that these neurodegenerative conditions could be overcome, or at least ameliorated, by the generation of new neurons. The location of the adult neurogenic zones in the hippocampus and the lateral ventricle wall, close to corpus callosum and neocortex, indicates strategic positions for potential repair processes. However, we also need to consider that the generation of new neurons is possibly involved in cognitive functions and could, therefore, be influenced by disease pathology. Moreover, aberrant neurogenic mechanisms could even be a part of the pathological events of neurodegenerative diseases. It is the scope of this review to summarize and analyze the recent data from neurogenesis research with respect to Alzheimer's disease and its animal models.
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| 6. |
- Lindberg, Olle R, et al.
(author)
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Characterization of Epidermal Growth Factor-Induced Dysplasia in the Adult Rat Subventricular Zone.
- 2012
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In: Stem cells and development. - : Mary Ann Liebert Inc. - 1557-8534 .- 1547-3287. ; 21:8, s. 1356-1366
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Journal article (peer-reviewed)abstract
- Epidermal growth factor (EGF) is a mitogen widely used when culturing adult neural stem cells in vitro. Although proliferative effects can also be observed in vivo, intracerebroventricular infusion of EGF has been found to counteract neuronal determination and promote glial differentiation instead. However, EGF receptor activation has different effects on the subventricular zone (SVZ) in mice and rats, possibly because of species differences in SVZ cell composition. Specifically in the rat, EGF stimulation of the SVZ induces the formation of hyperplastic polyps. The present study aims at molecular and morphological characterization of these subventricular polyps. Using immunohistochemistry, electron microscopy, and gene expression analysis, we demonstrate in hyperplastic EGF-induced polyps an upregulation in protein expression of Sox2, Olig2, GFAP, nestin, and vimentin. We found polyp-specific dysplastic changes in the form of coexpression of Sox2 and Olig2. This highly proliferative, Sox2/Olig2 coexpressing dysplastic cell type is >10-fold enriched in the hyperplastic polyps compared with control SVZ and most likely causes the polyp formation. Unique ultrastructural features of the polyps include a lack of ependymal cell lining as well as a large number of cells with large, light, ovoid nuclei and a cytoplasm with abundant ribosomes, whereas other polyp cells contain invaginated nuclei but fewer ribosomes. EGF also induced changes in the expression of Id genes Id1, Id2, and Id4 in the SVZ. Taken together, we here demonstrate dysplastic, structural, and phenotypical changes in the rat SVZ following EGF stimulation, which are specific to hyperplastic polyps.
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| 7. |
- Liu, Johan, 1960, et al.
(author)
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Stem Cell Growth and Migration on Nanofibrous Polymer Scaffolds and Micro-Fluidic Channels on Silicon-Chip
- 2009
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In: Proceedings of the 2009 Electronic Components and Technology Conference. - 0569-5503. - 9781424444762 ; , s. 1080-1085
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Conference paper (peer-reviewed)abstract
- Stem cell growth and migration on nanofibrous scaffolds and micro-fluidic channels on Silicon-Chip were studied by using neural stem cells isolated from adult rats' brain. Electrospinning and lithographic technique were used for developing nanofibrous-polylactic acid (PLA) and polyurethane (PU) based-scaffolds and micro-fluidic channels on Si-Chips respectively. Immunocytochemical and morphological analysis showed better cell-matrix interaction with profound adhesion, proliferation and migration on the developed scaffolds. Cell culture assay with microfluidic channel revealed the ability of developed channel system in guiding neuronal stem cell growth towards specified directions. These studies extend the possibility of using developed nanofibrous scaffolds and micro-fluidic channel system for future electrical signal transmission based on living neural stem cells.
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| 8. |
- Nyberg, Jenny, 1976, et al.
(author)
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Anxiety severity and cognitive function in primary care patients with anxiety disorder: a cross-sectional study.
- 2021
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In: BMC psychiatry. - : Springer Science and Business Media LLC. - 1471-244X. ; 21:1
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Journal article (peer-reviewed)abstract
- Deficits in cognitive performance are reported in patients with anxiety disorders, but research is limited and inconsistent. We aimed to investigate cross-sectional associations between cognitive function, with focus on executive function, and anxiety severity in primary care patients diagnosed with anxiety disorders.189 Swedish patients aged 18-65 years (31% men) with anxiety disorders diagnosed according to Mini International Neuropsychiatric Interview were included. Severity of anxiety was assessed using Beck Anxiety Inventory self-assessment scale. Digit span, block design and matrix reasoning tests from the Wechsler Adult Intelligence Scale IV, and the design fluency test from the Delis-Kaplan Executive Function System were used. Multivariable linear regression models were applied to investigate the relationship of anxiety severity and cognitive functioning. Comparisons were also performed to a normed non-clinical population, using the Wilcoxon signed rank test.More severe anxiety was associated with lower digit span test scores (R2 = 0.109, B = -0.040, p = 0.018), but not with block design, matrix reasoning or design fluency tests scores, after adjustment for comorbid major depression in a multivariable model. When compared to a normed population, patients with anxiety performed significantly lower on the block design, digit span forward, digit span sequencing and matrix reasoning tests.Severity of anxiety among patients with anxiety disorder was associated with executive functions related to working memory, independently of comorbid major depression, but not with lower fluid intelligence. A further understanding of the executive behavioral control in patients with anxiety could allow for more tailored treatment strategies including medication, therapy and interventions targeted to improve specific cognitive domains.
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| 9. |
- Qiu, L., et al.
(author)
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Less neurogenesis and inflammation in the immature than in the juvenile brain after cerebral hypoxia-ischemia
- 2007
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In: J Cereb Blood Flow Metab. - : SAGE Publications. - 0271-678X .- 1559-7016. ; 27:4, s. 785-94
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Journal article (peer-reviewed)abstract
- The effects of hypoxia-ischemia (HI) on proliferation and differentiation in the immature (postnatal day 9) and juvenile (postnatal day 21) mouse hippocampus were investigated by injecting bromodeoxyuridine (50 mg/kg) daily for 7 days after the insult and evaluating the labeling 5 weeks after HI. Phenotypic differentiation was evaluated using NeuN, Iba1, APC, and S100beta as markers of neurons, microglia, oligodendrocytes, and astrocytes, respectively. The basal proliferation, in particular neurogenesis, was higher in the immature than in the juvenile hippocampus. Hypoxia-ischemia did not increase neurogenesis significantly in the immature dentate gyrus (DG), but it increased several-fold in the juvenile brain, reaching the same level as in the normal, noninjured immature brain. This suggests that the immature hippocampus is already working at the top of its proliferative capacity and that even though basal neurogenesis decreased with age, the injury-induced generation of new neurons in the juvenile hippocampus could not increase beyond the basal level of the immature brain. Generation of glial cells of all three types after HI was significantly more pronounced in the cornu ammonis of the hippocampus region of the juvenile hippocampus. In the DG, only microglia production was greater in the juvenile brain. Increased microglia proliferation correlated with increased levels of the proinflammatory cytokines MCP-1 and IL-18 3 days after HI, indicating that the inflammatory response is stronger in the juvenile hippocampus. In summary, contrary to what has been generally assumed, our results indicate that the juvenile brain has a greater capacity for neurogenesis after injury than the immature brain.
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| 10. |
- Schäbitz, Wolf-Rüdiger, et al.
(author)
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Intravenous brain-derived neurotrophic factor enhances poststroke sensorimotor recovery and stimulates neurogenesis.
- 2007
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In: Stroke; a journal of cerebral circulation. - 1524-4628. ; 38:7, s. 2165-72
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Journal article (peer-reviewed)abstract
- BACKGROUND AND PURPOSE: The discovery of spontaneous neuronal replacement in the adult brain has shifted experimental stroke therapies toward a combined approach of preventing neuronal cell death and inducing neuronal plasticity. Brain-derived neurotrophic factor (BDNF) was shown to induce antiapoptotic mechanisms after stroke and to reduce infarct size and secondary neuronal cell death. Moreover, in intact animals, BDNF is a potent stimulator of adult neurogenesis. METHODS: The current study analyzed the effects of BDNF on induction of neuronal progenitor cell migration and sensorimotor recovery after cortical photothrombotic stroke. RESULTS: Daily intravenous bolus applications of BDNF during the first 5 days after stroke resulted in significantly improved sensorimotor scores up to 6 weeks. At the structural level, BDNF significantly increased neurogenesis in the dentate gyrus and enhanced migration of subventricular zone progenitor cells to the nearby striatum of the ischemic hemisphere. BDNF treatment could not, however, further stimulate progenitor cell recruitment to the cortex. CONCLUSIONS: These findings consolidate the role of BDNF as a modulator of neurogenesis in the brain and as an enhancer of long-term functional neurological outcome after cerebral ischemia.
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