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  • Qiu, L., et al. (författare)
  • Less neurogenesis and inflammation in the immature than in the juvenile brain after cerebral hypoxia-ischemia
  • 2007
  • Ingår i: J Cereb Blood Flow Metab. - 0271-678X. ; 27:4, s. 785-94
  • Tidskriftsartikel (refereegranskat)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.
  • Zhu, Changlian, 1964, et al. (författare)
  • Age-dependent regenerative responses in the striatum and cortex after hypoxia-ischemia.
  • 2009
  • Ingår i: Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism. - 1559-7016. ; 29:2, s. 342-54
  • Tidskriftsartikel (refereegranskat)abstract
    • Regenerative responses after hypoxia-ischemia (HI) were investigated in the immature (P9) and juvenile (P21) mouse striatum and cortex by postischemic 5-bromo-2-deoxyuridine labeling and phenotyping of labeled cells 4 weeks later. HI stimulated the formation of new cells in striatum and cortex in immature, growing brains (P9), but when brain growth was finished (P21) proliferation could be stimulated only in striatum, not in cortex. However, the relative increase was higher in P21 (460%) than P9 striatum (50%), though starting from a lower level at P21. Starting from this lower level, HI-induced proliferation in P21 striatum reached the same level as in P9 striatum, but not higher. Phenotyping revealed that low levels of neurogenesis were still present in nonischemic P9 cortex and striatum, but only in striatum at P21. Ischemia-induced neurogenesis was found only in P9 striatum. Ischemia-induced gliogenesis occurred in P9 and P21 striatum as well as P9 cortex, but not in P21 cortex. Hence, the regenerative response was stronger in striatum than cortex, and stronger in P9 than P21 cortex. The biggest ischemia-induced change was the 49-fold increase in P21 striatal microglia, and this was accompanied by increased inflammation, as judged by the size and numbers of CCL2- and interleukin-18-positive cells.Journal of Cerebral Blood Flow & Metabolism advance online publication, 5 November 2008; doi:10.1038/jcbfm.2008.124.
  • Åberg, Maria A I, 1972, et al. (författare)
  • Cardiovascular fitness is associated with cognition in young adulthood.
  • 2009
  • Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - 1091-6490.
  • Tidskriftsartikel (refereegranskat)abstract
    • During early adulthood, a phase in which the central nervous system displays considerable plasticity and in which important cognitive traits are shaped, the effects of exercise on cognition remain poorly understood. We performed a cohort study of all Swedish men born in 1950 through 1976 who were enlisted for military service at age 18 (N = 1,221,727). Of these, 268,496 were full-sibling pairs, 3,147 twin pairs, and 1,432 monozygotic twin pairs. Physical fitness and intelligence performance data were collected during conscription examinations and linked with other national databases for information on school achievement, socioeconomic status, and sibship. Relationships between cardiovascular fitness and intelligence at age 18 were evaluated by linear models in the total cohort and in subgroups of full-sibling pairs and twin pairs. Cardiovascular fitness, as measured by ergometer cycling, positively associated with intelligence after adjusting for relevant confounders (regression coefficient b = 0.172; 95% CI, 0.168-0.176). Similar results were obtained within monozygotic twin pairs. In contrast, muscle strength was not associated with cognitive performance. Cross-twin cross-trait analyses showed that the associations were primarily explained by individual specific, non-shared environmental influences (>/=80%), whereas heritability explained <15% of covariation. Cardiovascular fitness changes between age 15 and 18 y predicted cognitive performance at 18 y. Cox proportional-hazards models showed that cardiovascular fitness at age 18 y predicted educational achievements later in life. These data substantiate that physical exercise could be an important instrument for public health initiatives to optimize educational achievements, cognitive performance, as well as disease prevention at the society level.
  • Skau, Simon, et al. (författare)
  • Exhaustion disorder and altered brain activity in frontal cortex detected with fNIRS
  • 2021
  • Ingår i: Stress-the International Journal on the Biology of Stress. - : TAYLOR & FRANCIS LTD. - 1025-3890 .- 1607-8888. ; 24:1, s. 64-75
  • Tidskriftsartikel (refereegranskat)abstract
    • Patients with stress-related Exhaustion Disorder (ED) have problems with memory and executive function. These problems have been associated with deviant activity in prefrontal cortex (PFC). We investigated cognitive performance and functional activity in the PFC during prolonged mental activity in patients with ED (n = 20, 16 women) with a mean duration since diagnosis of 46 +/- 23 months in comparison to healthy individuals (n = 20, 12 women). A block of six neuropsychological tests was performed in a sequence that was repeated once. The brain imaging technique, functional near infrared spectroscopy (fNIRS) was used for all tests. There were no differences between the groups in terms of changes over time, i.e. difference between first and second test block. In the Stroop-Simon test, the controls showedhigher functional activity in the frontal cortex. In the left ventrolateral PFC, we observed an increased activity in controls in the incongruent compared to the congruent trials, whereas no changes were detected in the ED patient group. During processing speed tasks, only ED patients showed higher functional activity in right dorsolateral PFC. The ED patients reported lower subjective energy level and they also performed less well on a mental control task compared to healthy individuals. In conclusion, ED patients showed altered functional activity compared to controls, indicating that ED patients process information differently in the prefrontal cortex, but the functional activity did not change during the 21/2 hr procedure, as revealed by the test-retest design. Lay summary In this paper we show that patient with exhaustion disorder have a reduced functional activity in the prefrontal cortex. This functional activity was not affected by 2.5 hours mental activity.
  • Cooper-Kuhn, Christiana M, 1971, et al. (författare)
  • Decreased neurogenesis after cholinergic forebrain lesion in the adult rat.
  • 2004
  • Ingår i: Journal of neuroscience research. - 0360-4012. ; 77:2, s. 155-65
  • Tidskriftsartikel (refereegranskat)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.
  • Hellström, Nina, 1976, et al. (författare)
  • Unique gene expression patterns indicate microglial contribution to neural stem cell recovery following irradiation.
  • 2011
  • Ingår i: Molecular and cellular neurosciences. - 1095-9327. ; 46:4, s. 710-9
  • Tidskriftsartikel (refereegranskat)abstract
    • Ionizing radiation results in damage to neural stem cells and reduced neurogenesis. The aim of the present study was to determine intrinsic and extrinsic factors that influence neural stem cell survival following irradiation, using qPCR. Gene expression of hippocampal and SVZ neurospheres were analyzed following irradiation, and results demonstrated that irradiated hippocampal and SVZ stem cells displayed similar gene expression profiles for intrinsic genes. Irradiated microglia (extrinsic factor) isolated from the SVZ exhibited increased gene expression of growth factors involved in stem cell maintenance, proliferation, and survival. However, microglial genes in the irradiated hippocampus responded less favorably with respect to stem cell recovery. This might explain the superior recovery of SVZ compared to hippocampal stem cells following in vivo irradiation. In addition, our results show that a combination of growth factors, which were upregulated in SVZ microglia, increased the proliferation and decreased cell death of irradiated neurospheres in vitro.
  • Karlsson, Lars O, et al. (författare)
  • Constitutive PGC-1α Overexpression in Skeletal Muscle Does Not Contribute to Exercise-Induced Neurogenesis.
  • 2021
  • Ingår i: Molecular neurobiology. - 1559-1182. ; 58
  • Tidskriftsartikel (refereegranskat)abstract
    • Physical exercise can improve age-dependent decline in cognition, which in rodent is partly mediated by restoration of an age-dependent decline in neurogenesis. Exercise-inducible myokines in the circulation present a link in muscle-brain crosstalk. The transcription factor PGC-1α regulates the release of such myokines with neurotrophic properties into the circulation. We study how chronic muscular overexpression of PGC-1α could contribute to exercise-induced effects on hippocampal neurogenesis and if this effect could be enhanced in a running wheel paradigm. We used 3- and 11-month-old transgenic mice with overexpression of PGC-1α under the control of muscle creatinine kinase promoter (MCK-PGC-1α), which have a constitutively developed endurance muscle phenotype. Wild-type and MCK-PGC-1α mice were single housed with free access to running wheels. Four weeks of running in female animals increased the levels of newborn cells, immature neurons, and, for young animals, new mature neurons, compared to sedentary controls. However, no difference in these parameters was observed between wild-type and transgenic mice under sedentary or running conditions. Multiplex analysis of serum cytokines, chemokines, and myokines suggested several differences in serum protein concentrations between genotypes with musclin found to be significantly upregulated 4-fold in male MCK-PGC-1α animals. We conclude that constitutive muscular overexpression of PGC-1α, despite systemic changes and difference in serum composition, does not translate into exercise-induced effects on hippocampal neurogenesis, independent of the age of the animal. This suggests that chronic activation of PGC-1α in skeletal muscle is by itself not sufficient to mimic exercise-induced effects or to prevent decline of neurogenesis in aging.
  • Kempermann, G., et al. (författare)
  • Human Adult Neurogenesis: Evidence and Remaining Questions
  • 2018
  • Ingår i: Cell Stem Cell. - 1934-5909 .- 1875-9777. ; 23:1, s. 25-30
  • Tidskriftsartikel (refereegranskat)abstract
    • Renewed discussion about whether or not adult neurogenesis exists in the human hippocampus, and the nature and strength of the supporting evidence, has been reignited by two prominently published reports with opposite conclusions. Here, we summarize the state of the field and argue that there is currently no reason to abandon the idea that adult-generated neurons make important functional contributions to neural plasticity and cognition across the human lifespan.
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