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onic hemiparetic stroke.
Computerized cognitive training (CCT) is an emerging alternative intervention for stroke survivors.
This study investigated the effects of CCT on the cognition, activity, and participation of stroke survivors and compared the findings with those of match-dosed conventional cognitive training.
This randomized controlled trial included 39 patients with stroke who were divided into the intervention group (n = 19; receiving CCT with Lumosity software) and the control group (n = 20; receiving conventional cognitive training). Both the groups were trained for 20 min, twice a week, for 12 weeks. Participants were evaluated at pretest, posttest, and 4-week follow-up. Outcome measures included various cognitive function tests and the Stroke Impact Scale scores.
The CCT group exhibited significant improvement in global cognitive function (evaluated using the Mini-Mental State Examination and Montreal Cognitive Assessment) and specific cognitive domains verbal working memory (backward digit span), processing speed (Symbol Digit Modalities Test), and three MoCA subtests (attention, naming, and delayed recall). CCT exerted no significant effect on activities and participation. No significant between-group differences in changes in cognitive function were noted. However, CCT significantly improved cognitive function domains immediately after training, and these effects were sustained at the 4-week follow-up.
Cognitive function of individuals with chronic stroke could improve after administration of CCT. However, future studies with a more rigorous design and higher training dose are warranted to validate our findings.
Cognitive function of individuals with chronic stroke could improve after administration of CCT. However, future studies with a more rigorous design and higher training dose are warranted to validate our findings.
Limited evidence exists on whether subclinical hypothyroidism suggested by mildly elevated TSH levels affect neurodevelopment and growth in preterm infants. The objective of this study was to determine the association between gestational age adjusted TSH percentiles and neurodevelopmental outcomes among preterm infants.
Univariate linear regression analysis was conducted to determine, in infants born less than thirty-two weeks gestational age, the correlation between the TSH percentile on the last newborn screen and neurodevelopmental assessment scores and growth outcomes at eighteen to twenty-two months of corrected age.
Seventy-four patients were enrolled in the study with a mean gestational age of 28.8 weeks. There was no correlation between the last TSH percentile value and Bayley-III cognitive composite score or other neurodevelopmental or growth outcomes.
In a cohort of preterm infants, higher TSH percentiles suggesting potential subclinical hypothyroidism did not predict any adverse effect on neurodevelopmental or growth outcomes.
In a cohort of preterm infants, higher TSH percentiles suggesting potential subclinical hypothyroidism did not predict any adverse effect on neurodevelopmental or growth outcomes.
The new type of virus (SARS-CoV-2 or COVID-19) from Coronaviridae family, discovered in 2019, caused a global pandemic with several massive lock-downs around the globe. Science and politicians became the center of world attention, receiving many questions without having clear answers. The hopes of many rested on vaccine development, which was done fast, facing novel challenges such as the massive production and distribution for several billions of people.
In this paper, the global reaction to the pandemic is reviewed along with some critical comments.
Different groups, including nations, took part in global lockdowns, while vaccine development was running in parallel without having enough capacity for some of the biggest medical demands in history. This review will bring together views from all interested groups in this pandemic crisis.
The Western world waited too long (4 months), after the first case was confirmed in China, to introduce lock-down and safety measures. On the other side, vaccine develc is a test for all of us, which many governments, industries and non-state actors are failing. It is a perfect "general probe" to detect some of the weaknesses of the current structure of global health. If politics and science do not work together to make a global production plan for vaccines and learn from this pandemic, then all of the lives lost were for nothing.
The association between restless legs syndrome (RLS) and Parkinson's disease (PD) remains controversial, with epidemiologic and descriptive evidence suggesting some potential overlap while mechanistic/genetic studies suggesting relative independence of the conditions.
To examine a known, objectively measured endophenotype for RLS, periodic leg movements (PLMS) in sleep, in patients with PD and relate that objective finding to restless legs symptoms.
We performed polysomnography for one (n = 8) or two (n = 67) consecutive nights in 75 PD patients and examined the association of PLMS with restless legs symptoms.
We found no association between restless legs symptoms and PLMS in PD. Prevalence of both was similar to data reported previously in other PD samples.
We interpret these results as suggesting that restless legs symptoms in PD patients may represent a different phenomenon and pathophysiology than RLS in the non-PD population.
We interpret these results as suggesting that restless legs symptoms in PD patients may represent a different phenomenon and pathophysiology than RLS in the non-PD population.
Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by mutation in the HTT gene and characterized by involuntary movements as well as cognitive and behavioral impairment. Since its first description 150 years ago, studies have been reported worldwide. However, genetically confirmed cases have been scarce in Africa.
To describe the clinical and genetic aspects of HD in the Malian population.
Patients with HD phenotype and their relatives were enrolled after obtaining consent. Symptoms were assessed using the Total Motor Scale (TMS) of the United Huntington's Disease Rating Scale (UHDRS) and the Mini-Mental State Examination (MMSE). Brain imaging and blood tests were performed to exclude other causes. DNA was extracted for HTT sequencing.
Eighteen patients (13 families) with a HD phenotype were evaluated. A familial history of the disease was found in 84.6% with 55.5% of maternal transmission. The average length of the HTT CAG repeat was 43.6±11.5 (39-56) CAGs. The mean age at onset was 43.1±9.7years. Choreic movements were the predominant symptoms (100% of the cases) with an average TMS of 49.4±30.8, followed by cognitive impairment (average MMSE score 23.0±12.0) and psychiatric symptoms with 22.2% and 44.4%, respectively.
This is one of the largest HD cohorts reported in Africa. Increasing access to genetic testing could uncover many other HD cases and disease-modifying genetic variants. Future haplotype and psychosocial studies may inform the origin of the Malian mutation and the impact of the disease on patients and their relatives.
This is one of the largest HD cohorts reported in Africa. Increasing access to genetic testing could uncover many other HD cases and disease-modifying genetic variants. Future haplotype and psychosocial studies may inform the origin of the Malian mutation and the impact of the disease on patients and their relatives.
Huntington's disease (HD) is a neurodegenerative disorder characterized by synaptic dysfunction and loss of white matter volume especially in the striatum of the basal ganglia and to a lesser extent in the cerebral cortex. Studies investigating heterogeneity between synaptic and non-synaptic mitochondria have revealed a pronounced vulnerability of synaptic mitochondria, which may lead to synaptic dysfunction and loss.
As mitochondrial dysfunction is a hallmark of HD pathogenesis, we investigated synaptic mitochondrial function from striatum and cortex of the transgenic R6/2 mouse model of HD.
We assessed mitochondrial volume, ROS production, and antioxidant levels as well as mitochondrial respiration at different pathological stages.
Our results reveal that striatal synaptic mitochondria are more severely affected by HD pathology than those of the cortex. Striatal synaptosomes of R6/2 mice displayed a reduction in mitochondrial mass coinciding with increased ROS production and antioxidants levels indicating prolonged oxidative stress. Furthermore, synaptosomal oxygen consumption rates were significantly increased during depolarizing conditions, which was accompanied by a marked increase in mitochondrial proton leak of the striatal synaptosomes, indicating synaptic mitochondrial stress.
Overall, our study provides new insight into the gradual changes of synaptic mitochondrial function in HD and suggests compensatory mitochondrial actions to maintain energy production in the HD brain, thereby supporting that mitochondrial dysfunction do indeed play a central role in early disease progression of HD.
Overall, our study provides new insight into the gradual changes of synaptic mitochondrial function in HD and suggests compensatory mitochondrial actions to maintain energy production in the HD brain, thereby supporting that mitochondrial dysfunction do indeed play a central role in early disease progression of HD.
Participants in Alzheimer's disease (AD) prevention studies are generally required to enroll with a study partner; this requirement constitutes a barrier to enrollment for some otherwise interested individuals. Analysis of dyads enrolled in actual AD trials suggests that the study partner requirement shapes the population under study.
To understand if individuals can identify someone to serve as their study partner and whether they would be willing to ask that individual.
We conducted semi-structured interviews with cognitively unimpaired, English-speaking older adults who had previously expressed interest in AD research by signing up for a research registry. We also interviewed their likely study partners. Audio-recorded interviews were transcribed and coded in an iterative, team-based process guided by a content analysis approach.
We interviewed 60 potential research participants and 17 likely study partners. Most potential participants identified one or two individuals they would be willing to ask to serve as their study partner. Interviewees saw value in the study partner role but also understood it to entail burdens that could make participation as a study partner more difficult. The role was seen as relatively more burdensome for individuals in the workforce or with family responsibilities. Calls from the researcher to discuss the importance of the role and the possibility of virtual visits were identified as potential strategies for increasing study partner availability.
Efforts to increase recruitment, particularly representative recruitment, of participants for AD prevention studies should reduce barriers to participation by thoughtfully designing the study partner role.
Efforts to increase recruitment, particularly representative recruitment, of participants for AD prevention studies should reduce barriers to participation by thoughtfully designing the study partner role.
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