| 91. |
- Skau, Simon, et al.
(författare)
-
Proactive cognitive control, mathematical cognition and functional activity in the frontal and parietal cortex in primary school children: An fNIRS study
- 2022
-
Ingår i: Trends in Neuroscience and Education. - : Elsevier BV. - 2452-0837 .- 2211-9493. ; 28
-
Tidskriftsartikel (refereegranskat)abstract
- Understanding how children acquire mathematical abilities is fundamental to planning mathematical schooling. This study focuses on the relationships between mathematical cognition, cognition in general and neural foundation in 8 to 9-year-old children. We used additive mathematics tests, cognitive tests determining the tendency for proactive and reactive problem solving and functional near-infrared spectroscopy (fNIRS) for functional brain imaging. The ability to engage in pro-active control had a stronger association with mathematical performance than other cognitive abilities, such as processing speed, sustained attention and pattern recognition. The fNIRS method identified differences between proactive and reactive control, i.e., the more proactive the children were, the greater the increase in oxygenated hemoglobin in the left lateral prefrontal cortex during reactive beneficiary situations. During a text-based task involving additive reasoning, increased activity in the dorsal medial prefrontal cortex was detected compared to a similar task with supportive spatial-geometric information.
|
|
| 92. |
- Skau, Simon, et al.
(författare)
-
Segregation over time in functional networks in prefrontal cortex for individuals suffering from pathological fatigue after traumatic brain injury.
- 2022
-
Ingår i: Frontiers in neuroscience. - : Frontiers Media SA. - 1662-4548 .- 1662-453X. ; 16
-
Tidskriftsartikel (refereegranskat)abstract
- Pathological fatigue is present when fatigue is perceived to continually interfere with everyday life. Pathological fatigue has been linked with a dysfunction in the cortico-striatal-thalamic circuits. Previous studies have investigated measures of functional connectivity, such as modularity to quantify levels of segregation. However, previous results have shown both increases and decreases in segregation for pathological fatigue. There are multiple factors why previous studies might have differing results, including: (i) Does the functional connectivity of patients with pathological fatigue display more segregation or integration compared to healthy controls? (ii) Do network properties differ depending on whether patients with pathological fatigue perform a task compared to periods of rest? (iii) Are the brain networks of patients with pathological fatigue and healthy controls differently affected by prolonged cognitive activity? We recruited individuals suffering from pathological fatigue after mild traumatic brain injury (n = 20) and age-matched healthy controls (n = 20) to perform cognitive tasks for 2.5 h. We used functional near-infrared spectroscopy (fNIRS) to assess hemodynamic changes in the frontal cortex. The participants had a resting state session before and after the cognitive test session. Cognitive testing included the Digit Symbol Coding test at the beginning and the end of the procedure to measure processing speed. We conducted an exploratory network analysis on these resting state and Digit Symbol Coding sessions with no a priori hypothesis relating to how patients and controls differ in their functional networks since previous research has found results in both directions. Our result showed a Group vs. Time interaction (p = 0.026, η p 2 = 0.137), with a post hoc test revealing that the TBI patients developed higher modularity toward the end of the cognitive test session. This work helps to identify how functional networks differ under pathological fatigue compared to healthy controls. Further, it shows how the functional networks dynamically change over time as the patient performs tasks over a time scale that affect their fatigue level.
|
|
| 93. |
|
|
| 94. |
- Torner, Luz, et al.
(författare)
-
Prolactin prevents chronic stress-induced decrease of adult hippocampal neurogenesis and promotes neuronal fate.
- 2009
-
Ingår i: The Journal of neuroscience : the official journal of the Society for Neuroscience. - 1529-2401. ; 29:6, s. 1826-33
-
Tidskriftsartikel (refereegranskat)abstract
- Chronic exposure to stress results in a reduction of hippocampal neurogenesis and of hippocampal volume. We examined whether prolactin (PRL), a regulator of the stress response and stimulator of neurogenesis in the subventricular zone, influences neurogenesis in the hippocampal dentate gyrus (DG) of chronically stressed adult C57BL/6 male mice. Chronically stressed (4 h daily immobilization for 21 d) or nonstressed mice were treated with either ovine PRL or vehicle between days 1-14. BrdU was injected daily between days 1-7 to evaluate cell survival and fate, or twice on day 21 to evaluate cell proliferation. Hippocampal cell proliferation was unchanged by either stress exposure or PRL at the end of the treatments. In contrast, the number of cells in the DG that incorporated BrdU during the first phase of the experiment and survived to the end of the experiment was decreased in vehicle-treated stressed mice compared with PRL- or vehicle-treated nonstressed control mice. Stressed animals receiving PRL had significantly more BrdU-labeled cells than vehicle-treated stressed mice at this time point. Cell fate analysis revealed a higher percentage of neurons in PRL- compared with vehicle-treated stressed mice. The results demonstrate that PRL protects neurogenesis in the DG of chronically stressed mice and promotes neuronal fate.
|
|
| 95. |
- Vive, Sara, et al.
(författare)
-
Enriched, Task-Specific Therapy in the Chronic Phase After Stroke: An Exploratory Study.
- 2020
-
Ingår i: Journal of neurologic physical therapy : JNPT. - 1557-0584. ; 44:2, s. 145-155
-
Tidskriftsartikel (refereegranskat)abstract
- There is a need to translate promising basic research about environmental enrichment to clinical stroke settings. The aim of this study was to assess the effectiveness of enriched, task-specific therapy in individuals with chronic stroke.This is an exploratory study with a within-subject, repeated-measures design. The intervention was preceded by a baseline period to determine the stability of the outcome measures. Forty-one participants were enrolled at a mean of 36 months poststroke. The 3-week intervention combined physical therapy with social and cognitive stimulation inherent to environmental enrichment. The primary outcome was motor recovery measured by Modified Motor Assessment Scale (M-MAS). Secondary outcomes included balance, walking, distance walked in 6 minutes, grip strength, dexterity, and multiple dimensions of health. Assessments were made at baseline, immediately before and after the intervention, and at 3 and 6 months.The baseline measures were stable. The 39 participants (95%) who completed the intervention had increases of 2.3 points in the M-MAS UAS and 5 points on the Berg Balance Scale (both P < 0.001; SRM >0.90), an improvement of comfortable and fast gait speed of 0.13 and 0.23 m/s, respectively. (P < 0.001; SRM = 0.88), an increased distance walked over 6 minutes (24.2 m; P < 0.001; SRM = 0.64), and significant improvements in multiple dimensions of health. The improvements were sustained at 6 months.Enriched, task-specific therapy may provide durable benefits across a wide spectrum of motor deficits and impairments after stroke. Although the results must be interpreted cautiously, the findings have implications for enriching strategies in stroke rehabilitation.Video Abstract available for more insights from the authors (see the Video, Supplemental Digital Content 1, available at: http://links.lww.com/JNPT/A304).
|
|
| 96. |
- Wallin, Anders, 1950, et al.
(författare)
-
Cognitive medicine - a new approach in health care science.
- 2018
-
Ingår i: BMC psychiatry. - : Springer Science and Business Media LLC. - 1471-244X. ; 18:1
-
Tidskriftsartikel (refereegranskat)abstract
- The challenges of today's society call for more knowledge about how to maintain all aspects of cognitive health, such as speed/attention, memory/learning, visuospatial ability, language, executive capacity and social cognition during the life course.Medical advances have improved treatments of numerous diseases, but the cognitive implications have not been sufficiently addressed. Disability induced by cognitive dysfunction is also a major issue in groups of patients not suffering from Alzheimer's disease or related disorders. Recent studies indicate that several negative lifestyle factors can contribute to the development of cognitive impairment, but intervention and prevention strategies have not been implemented. Disability due to cognitive failure among the workforce has become a major challenge. Globally, the changing aging pyramid results in increased prevalence of cognitive disorders, and the diversity of cultures influences the expression, manifestation and consequences of cognitive dysfunction.Major tasks in the field of cognitive medicine are basic neuroscience research to uncover diverse disease mechanisms, determinations of the prevalence of cognitive dysfunction, health-economical evaluations, and intervention studies. Raising awareness for cognitive medicine as a clinical topic would also highlight the importance of specialized health care units for an integrative approach to the treatment of cognitive dysfunctions.
|
|
| 97. |
- Winner, Beate, et al.
(författare)
-
Dopaminergic lesion enhances growth factor-induced striatal neuroblast migration.
- 2008
-
Ingår i: Journal of neuropathology and experimental neurology. - : Oxford University Press (OUP). - 0022-3069 .- 1554-6578. ; 67:2, s. 105-16
-
Tidskriftsartikel (refereegranskat)abstract
- Adult neurogenesis persists in the subventricular zone and is decreased in Parkinson disease (PD). The therapeutic potential of neurogenesis in PD requires understanding of mechanisms of 1) neural stem cell generation; 2) their guidance to the lesion site; and 3) the environment that enables neuronal differentiation, survival, and functional integration. We examined the combined intraventricular infusion of epidermal growth factor (EGF) and fibroblast growth factor 2 (FGF-2) in a 6-hydroxydopamine-induced rodent model of PD. Epidermal growth factor and FGF-2 induced a massive increase in cell proliferation and in numbers of doublecortin-expressing neuroblasts in the subventricular zone. These growth factors also increased dopaminergic neurogenesis in the olfactory bulb and promoted the migration of newly generated neuroblasts from the subventricular zone into the adjacent striatum. The effects of EGF and FGF-2 were present in unlesioned animals but were dramatically enhanced in 6-hydroxydopamine-lesioned animals.These findings suggest that newly generated neuroblasts may be redirected to the region of dopaminergic deficit, and that EGF and FGF-2 can enhance dopaminergic neurogenesis in the olfactory bulb but not in the striatum. Similar mechanisms may be involved in the increased numbers of dopaminergic neurons observed in the olfactory bulbs of PD patients and their functional olfactory deficits.
|
|
| 98. |
- Winner, Beate, et al.
(författare)
-
Human wild-type alpha-synuclein impairs neurogenesis.
- 2004
-
Ingår i: Journal of neuropathology and experimental neurology. - 0022-3069. ; 63:11, s. 1155-66
-
Tidskriftsartikel (refereegranskat)abstract
- Neurodegenerative diseases classified as synucleinopathies are characterized by alpha-synuclein inclusions. In these disorders, alpha-synuclein accumulates within glial or neuronal cells in the brain including regions of adult neurogenesis. We hypothesized a pathophysiological role for alpha-synuclein in newly generated cells of the adult brain and in this study examined regions of neurogenesis in adult mice overexpressing human wild-type alpha-synuclein under the control of the platelet-derived growth factor promoter. The number of proliferating cells and the fate of newly generated cells were analyzed in the olfactory bulb system and in the hippocampal dentate gyrus. There were no effects on proliferation detectable; however, significantly less neurogenesis and fewer neurons were observed in the olfactory bulb as well as in the hippocampus of adult human alpha-synuclein mice compared to control littermates. This effect was almost exclusively due to diminished survival of neuronal precursors in the target regions of neurogenesis. Our data imply that the finely tuned equilibrium of neuronal cell birth and death in neurogenic regions may be altered in human alpha-synuclein-overexpressing mice. We hypothesize that reduced adult neurogenesis in the olfactory bulb may contribute to olfactory deficits in neurodegenerative disorders associated with alpha-synuclein inclusions.
|
|
| 99. |
- Winner, Beate, et al.
(författare)
-
Striatal deafferentation increases dopaminergic neurogenesis in the adult olfactory bulb.
- 2006
-
Ingår i: Experimental neurology. - : Elsevier BV. - 0014-4886. ; 197:1, s. 113-21
-
Tidskriftsartikel (refereegranskat)abstract
- Dopaminergic loss is known to be one of the major hallmarks of Parkinson disease (PD). In addition to its function as a neurotransmitter, dopamine plays significant roles in developmental and adult neurogenesis. Both dopaminergic deafferentation and stimulation modulate proliferation in the subventricular zone (SVZ)/olfactory bulb system as well as in the hippocampus. Here, we study the impact of 6-hydroxydopamine (6-OHDA) lesions to the medial forebrain bundle on proliferation and neuronal differentiation of newly generated cells in the SVZ/olfactory bulb axis in adult rats. Proliferation in the SVZ decreased significantly after dopaminergic deafferentation. However, the number of neural progenitor cells expressing the proneuronal cell fate determinant Pax-6 increased in the SVZ. Survival and quantitative cell fate analysis of newly generated cells revealed that 6-OHDA lesions induced opposite effects in the two different regions of neurogenesis in the olfactory bulb: a transient decrease in the granule cell layer contrasts to a sustained increase of newly generated neurons in the glomerular layer. These data point towards a shift in the ratio of newly generated interneurons in the olfactory bulb layers. Dopaminergic neurogenesis in the glomerular layer tripled after lesioning and consistent with this finding, the total number of tyrosine hydroxylase (TH)-positive cells increased. Thus, loss of dopaminergic input to the SVZ led to a distinct cell fate decision towards stimulation of dopaminergic neurogenesis in the olfactory bulb glomerular layer. This study supports the accumulating evidence that neurotransmitters play a crucial role in determining survival and differentiation of newly generated neurons.
|
|
| 100. |
- Zandén, Carl, 1984, et al.
(författare)
-
Stem cell responses to plasma surface modified electrospun polyurethane scaffolds.
- 2014
-
Ingår i: Nanomedicine: Nanotechnology, Biology and Medicine. - : Elsevier BV. - 1549-9634 .- 1549-9642. ; 10:5, s. 949-958
-
Tidskriftsartikel (refereegranskat)abstract
- The topographical effects from functional materials on stem cell behavior are currently of interest in tissue engineering and regenerative medicine. Here we investigate the influence of argon, oxygen, and hydrogen plasma surface modification of electrospun polyurethane fibers on human embryonic stem cell (hESC) and rat postnatal neural stem cell (NSC) responses. The plasma gases were found to induce three combinations of fiber surface functionalities and roughness textures. On randomly oriented fibers, plasma treatments lead to substantially increased hESC attachment and proliferation as compared to native fibers. Argon plasma was found to induce the most optimal combination of surface functionality and roughness for cell expansion. Contact guided migration of cells and alignment of cell processes were observed on aligned fibers. Neuronal differentiation around 5% was found for all samples and was not significantly affected by the induced variations of surface functional group distribution or individual fiber topography.
|
|
