dorsolateral cortex
Recently Published Documents


TOTAL DOCUMENTS

18
(FIVE YEARS 7)

H-INDEX

4
(FIVE YEARS 1)

2022 ◽  
Vol 13 ◽  
Author(s):  
Mosi Li ◽  
Akihiro Kitamura ◽  
Joshua Beverley ◽  
Juraj Koudelka ◽  
Jessica Duncombe ◽  
...  

Large vessel disease and carotid stenosis are key mechanisms contributing to vascular cognitive impairment (VCI) and dementia. Our previous work, and that of others, using rodent models, demonstrated that bilateral common carotid stenosis (BCAS) leads to cognitive impairment via gradual deterioration of the neuro-glial-vascular unit and accumulation of amyloid-β (Aβ) protein. Since brain-wide drainage pathways (glymphatic) for waste clearance, including Aβ removal, have been implicated in the pathophysiology of VCI via glial mechanisms, we hypothesized that glymphatic function would be impaired in a BCAS model and exacerbated in the presence of Aβ. Male wild-type and Tg-SwDI (model of microvascular amyloid) mice were subjected to BCAS or sham surgery which led to a reduction in cerebral perfusion and impaired spatial learning acquisition and cognitive flexibility. After 3 months survival, glymphatic function was evaluated by cerebrospinal fluid (CSF) fluorescent tracer influx. We demonstrated that BCAS caused a marked regional reduction of CSF tracer influx in the dorsolateral cortex and CA1-DG molecular layer. In parallel to these changes increased reactive astrogliosis was observed post-BCAS. To further investigate the mechanisms that may lead to these changes, we measured the pulsation of cortical vessels. BCAS impaired vascular pulsation in pial arteries in WT and Tg-SwDI mice. Our findings show that BCAS influences VCI and that this is paralleled by impaired glymphatic drainage and reduced vascular pulsation. We propose that these additional targets need to be considered when treating VCI.


2021 ◽  
Vol 12 ◽  
Author(s):  
Alberto José Mimenza-Alvarado ◽  
Sara Gloria Aguilar-Navarro ◽  
Francisco M. Martinez-Carrillo ◽  
Alma E. Ríos-Ponce ◽  
Gabriel Villafuerte

Background: Alzheimer's disease (AD) animal models have shown a reduced gamma power in several brain areas, and induction of these oscillations by non-invasive methods has been shown to modify several pathogenic mechanisms of AD. In humans, the application of low-intensity magnetic fields has shown to be able to produce neural entrainment at the magnetic pulse frequency, making it useful to induce gamma frequencies.Objective: The aim of this study was to assess if the application of fast gamma magnetic stimulation (FGMS) over the left prefrontal dorsolateral cortex would be a safe and well-tolerated intervention that could potentially improve cognitive scores in subjects with mild cognitive impairment and mild AD.Methods: In these randomized, double-blind, sham-controlled study, participants were assigned to either receive daily sessions two times a day of active or sham FGMS for 6 months. Afterward, measurements of adverse effects, cognition, functionality, and depression were taken.Results: Thirty-four patients, 17 in each group, were analyzed for the primary outcome. FGMS was adequately tolerated by most of the subjects. Only four patients from the active FGMS group (23.52%) and one patient from the sham FGMS group (5.88%) presented any kind of adverse effects, showing no significant difference between groups. Nevertheless, FGMS did not significantly change cognitive, functionality, or depressive evaluations.Conclusion: FGMS over the left prefrontal dorsolateral cortex applied twice a day for 6 months resulted to be a viable intervention that can be applied safely directly from home without supervision of a healthcare provider. However, no statistically significant changes in cognitive, functionality, or depression scores compared to sham stimulation were observed.Clinical Trial Registration:www.ClinicalTrials.gov, Identifier: NCT03983655, URL: https://clinicaltrials.gov/ct2/show/NCT03983655.


2021 ◽  
Author(s):  
Mosi Li ◽  
Akihiro Kitamura ◽  
Joshua Beverley ◽  
Juraj Koudelka ◽  
Jessica Duncombe ◽  
...  

Large vessel disease and carotid stenosis are key mechanisms contributing to vascular cognitive impairment (VCI) and dementia. Our previous work, and that of others, using rodent models, demonstrated that bilateral common carotid stenosis (BCAS) leads to cognitive impairment via gradual deterioration of the glial-vascular unit and accumulation of amyloid-β (Aβ) protein. Since brain-wide drainage pathways (glymphatic) for waste clearance, including Aβ removal, have been implicated in the pathophysiology of VCI via glial mechanisms, we hypothesized that glymphatic function would be impaired in a BCAS model and exacerbated in the presence of Aβ. Male wild-type and Tg-SwDI (model of microvascular amyloid) mice were subjected to BCAS or sham surgery which led to a reduction in cerebral perfusion and impaired spatial learning and memory. After 3 months survival, glymphatic function was evaluated by cerebrospinal fluid (CSF) fluorescent tracer influx. We demonstrated that BCAS caused a marked regional reduction of CSF tracer influx in the dorsolateral cortex and CA1-DG molecular layer. In parallel to these changes increased reactive astrogliosis was observed post-BCAS. To further investigate the mechanisms that may lead to these changes, we measured the pulsation of cortical vessels using two-photon microscopy. BCAS impaired vascular pulsation in pial arteries in WT and Tg-SwDI mice. Since our findings show that BCAS may influence VCI by impaired glymphatic drainage and reduced vascular pulsation we propose that these additional targets need to be considered when treating VCI.


2021 ◽  
Vol 23 (1) ◽  
pp. 15-20
Author(s):  
Ahmed Genena ◽  
Amr Abouelela ◽  
Ramy Mohamed ◽  
Ahmed Nagi

Background. This study investigated the clinical outcomes of fixation of displaced middle-third clavicular fractures using percutaneous elastic stable intramedullary nails. Material and methods. This study included sixty patients with a mean age of 26.40 ± 8.91 years (16-53 years) presented with a displaced middle third fracture of the clavicle. According to the Robinson classification, 48 cases (80%) were type 2B1, 9 cases (15%) type 2B2 and 3 case (5%) 2A1. All cases were treated by elastic intramedullary nails and followed up for at least 12 months. Results. At the end of the twelve months’ follow-up period, the mean Constant Shoulder score was 95.70 ± 13.55, ranging from 48 to 100. 54 patients (90%) had excellent results, 3 patients (5%) had an adequate result and 3 patients (5%) had a poor result. There was a statistically significant relationship between the final score and age and associated medical conditions. Conclusions. 1. Elastic Stable Intramedullary Nailing is an image-dependent procedure indicated best for young medically free athletes with simple 2-part middle third clavicle fracture. 2. Hammering is not recommended to avoid dorsolateral cortex perforation. 3. The most common complication is medial skin irritation because of the subcutaneous position of the clavicle as well as the sharp end of the cut nail.


Author(s):  
Marta Krzyżanowska ◽  
Krzysztof Rębała ◽  
Johann Steiner ◽  
Michał Kaliszan ◽  
Dorota Pieśniak ◽  
...  

AbstractPrefrontal cortical regions play a key role in behavioural regulation, which is profoundly disturbed in suicide. The study was carried out on frozen cortical samples from the anterior cingulate cortex (dorsal and ventral parts, ACd and ACv), the orbitofrontal cortex (OFC), and the dorsolateral cortex (DLC) obtained from 20 suicide completers (predominantly violent) with unknown psychiatric diagnosis and 21 non-suicidal controls. The relative level of ribosomal RNA (rRNA) as a marker of the transcriptional activity of ribosomal DNA (rDNA) was evaluated bilaterally in prefrontal regions mentioned above (i.e. in eight regions of interest, ROIs) by reverse transcription and quantitative polymerase chain reaction (RT-qPCR). The overall statistical analysis revealed a decrease in rDNA activity in suicide victims versus controls, particularly in male subjects. Further ROI-specific post hoc analyses revealed a significant decrease in this activity in suicides compared to non-suicides in five ROIs. This effect was accentuated in the ACv, where it was observed bilaterally. Our findings suggest that decreased rDNA transcription in the prefrontal cortex plays an important role in suicide pathogenesis and corresponds with our previous morphometric analyses of AgNOR-stained neurons.


2020 ◽  
Author(s):  
Oswald Steward ◽  
Kelly M Yee ◽  
Mariajose Metcalfe ◽  
Rafer Willenberg ◽  
Juan Luo ◽  
...  

Abstract Rostro-caudal specificity of corticospinal tract (CST) projections from different areas of the cortex was assessed by retrograde labeling with fluorogold and retrograde transfection following retro-AAV/Cre injection into the spinal cord of tdT reporter mice. Injections at C5 led to retrograde labeling of neurons throughout forelimb area of the sensorimotor cortex and a region in the dorsolateral cortex near the barrel field (S2). Injections at L2 led to retrograde labeling of neurons in the posterior sensorimotor cortex (hindlimb area) but not the dorsolateral cortex. With injections of biotinylated dextran amine (BDA) into the main sensorimotor cortex (forelimb region), labeled axons terminated selectively at cervical levels. With BDA injections into caudal sensorimotor cortex (hindlimb region), labeled axons passed through cervical levels without sending collaterals into the gray matter and then elaborated terminal arbors at thoracic sacral levels. With BDA injections into the dorsolateral cortex near the barrel field, labeled axons terminated at high cervical levels. Axons from medial sensorimotor cortex terminated primarily in intermediate laminae and axons from lateral sensorimotor cortex terminated primarily in laminae III–V of the dorsal horn. One of the descending pathways seen in rats (the ventral CST) was not observed in most mice.


2019 ◽  
Vol 29 (4) ◽  
pp. 1706-1718 ◽  
Author(s):  
Ayman Alzu’bi ◽  
Jihane Homman-Ludiye ◽  
James A Bourne ◽  
Gavin J Clowry

Abstract The current model, based on rodent data, proposes that thalamocortical afferents (TCA) innervate the subplate towards the end of cortical neurogenesis. This implies that the laminar identity of cortical neurons is specified by intrinsic instructions rather than information of thalamic origin. In order to determine whether this mechanism is conserved in the primates, we examined the growth of thalamocortical (TCA) and corticofugal afferents in early human and monkey fetal development. In the human, TCA, identified by secretagogin, calbindin, and ROBO1 immunoreactivity, were observed in the internal capsule of the ventral telencephalon as early as 7–7.5 PCW, crossing the pallial/subpallial boundary (PSB) by 8 PCW before the calretinin immunoreactive corticofugal fibers do. Furthermore, TCA were observed to be passing through the intermediate zone and innervating the presubplate of the dorsolateral cortex, and already by 10–12 PCW TCAs were occupying much of the cortex. Observations at equivalent stages in the marmoset confirmed that this pattern is conserved across primates. Therefore, our results demonstrate that in primates, TCAs innervate the cortical presubplate at earlier stages than previously demonstrated by acetylcholinesterase histochemistry, suggesting that pioneer thalamic afferents may contribute to early cortical circuitry that can participate in defining cortical neuron phenotypes.


2018 ◽  
Vol 24 (1) ◽  
pp. 134-148
Author(s):  
Larysa Zasiekina

Developmental Dyslexia is a specific reading and writing disability despite of normal intelligence, educational instruction and socio-cultural opportunity. Attention-deficit hyperactivity disorder (ADHD) is a condition that affects millions of children and often persists into adulthood. ADHD can include a combination of problems, such as difficulty sustaining attention, hyperactivity and impulsive behaviour. The frequent co-morbidity of dyslexia and ADHD posed the question of the issue whether common causal mechanism can be identified. There are several causal explanation of the co-morbidity between dyslexia and ADHD. Firstly, the symptoms of ADHD associated with dyslexia are a secondary consequence of reading problems (‘phenocopy’ hypothesis). However, the finding could not substantiate in later studies. Therefore, the first aim the present research is to identify the frequency and nature of co-morbidity between dyslexics and ADHD children. Developmental Dyslexia and ADHD are some of the most complex developmental disorders that affect children population. These are some of the conditions which affect the ability of the children to benefit from education and engage with surroundings in a meaningful manner. These conditions may occur in isolation, but many times they overlap. These overlapping conditions are termed as co-morbidity, and this may reflect the greater difficulties experienced by the children with a combination of deficits. However, the underlying reasons for these and the subsequent behavioural deficits are not well understood. Thus, the second major goal of the article is to investigate neuro-cognitive underpinning of dyslexia and ADHD. Neuro-cognitive basis presented by prefrontal dorsolateral cortex dysfunction was revealed and executive functions presented by problems in phonological working memory, initiating the activity and multitasking were established.


2016 ◽  
Vol 87 (2) ◽  
pp. 105-116 ◽  
Author(s):  
Laura D. Reyes ◽  
Tessa Harland ◽  
Roger L. Reep ◽  
Chet C. Sherwood ◽  
Bob Jacobs

The current study investigates neuron morphology in presumptive primary somatosensory (S1) and primary visual (V1) cortices of the Florida manatee (Trichechus manatus latirostris) as revealed by Golgi impregnation. Sirenians, including manatees, have an aquatic lifestyle, a large body size, and a relatively large lissencephalic brain. The present study examines neuron morphology in 3 cortical areas: in S1, dorsolateral cortex area 1 (DL1) and cluster cortex area 2 (CL2) and in V1, dorsolateral cortex area 4 (DL4). Neurons exhibited a variety of morphological types, with pyramidal neurons being the most common. The large variety of neuron types present in the manatee cortex was comparable to that seen in other eutherian mammals, except for rodents and primates, where pyramid-shaped neurons predominate. A comparison between pyramidal neurons in S1 and V1 indicated relatively greater dendritic branching in S1. Across all 3 areas, the dendritic arborization pattern of pyramidal neurons was also similar to that observed previously in the afrotherian rock hyrax, cetartiodactyls, opossums, and echidnas but did not resemble the widely bifurcated dendrites seen in the large-brained African elephant. Despite adaptations for an aquatic environment, manatees did not share specific neuron types such as tritufted and star-like neurons that have been found in cetaceans. Manatees exhibit an evolutionarily primitive pattern of cortical neuron morphology shared with most other mammals and do not appear to have neuronal specializations for an aquatic niche.


Sign in / Sign up

Export Citation Format

Share Document