Brain communications最新文献

{"title":"Vaccination prior to SARS-CoV-2 infection does not affect the neurologic manifestations of long COVID.","authors":"Shreya Mukherjee, Tracey Singer, Aditi Venkatesh, Natasha A Choudhury, Gina S Perez Giraldo, Millenia Jimenez, Janet Miller, Melissa Lopez, Barbara A Hanson, Aasheeta P Bawa, Ayush Batra, Eric M Liotta, Igor J Koralnik","doi":"10.1093/braincomms/fcae448","DOIUrl":"https://doi.org/10.1093/braincomms/fcae448","url":null,"abstract":"<p><p>Persistent symptoms after COVID-19 constitute the long COVID syndrome, also called post-acute sequelae of SARS-CoV-2 infection (PASC). COVID-19 vaccines reduce the gravity of ensuing SARS-CoV-2 infections. However, whether vaccines also have an impact on PASC remain unknown. We investigated whether vaccination prior to infection alters the subsequent neurologic post-acute sequelae of SARS-CoV-2 infection (Neuro-PASC). We studied prospectively the first consecutive 200 post-hospitalization Neuro-PASC (PNP) and 1100 non-hospitalized Neuro-PASC (NNP) patients evaluated at our neuro-COVID-19 clinic between May 2020 and January 2023. Among PNP patients, 87% had a pre-vaccination infection and 13% had a breakthrough infection post-vaccination. Among the NNP patients, 70.7% had a pre-vaccination infection and 29.3% had a breakthrough infection. Both PNP and NNP breakthrough infection patients had more frequent pre-existing depression/anxiety than their respective pre-vaccination infection groups, and NNP breakthrough infection patients also had more frequent comorbidities of headache, lung and gastrointestinal diseases than the NNP pre-vaccination infection group. An average of 10 months after symptom onset, the three most common neurological symptoms for PNP patients were brain fog (86.5%), numbness/tingling (56.5%) and headache (56.5%). Of all Neuro-PASC symptoms, PNP breakthrough infection more frequently reported anosmia compared to PNP pre-vaccination infection patients (69.2 versus 37.9%; <i>P</i> = 0.005). For NNP patients, the three most common neurological symptoms were brain fog (83.9%), headache (70.9%) and dizziness (53.8%). NNP pre-vaccination infection reported anosmia (56.6 versus 39.1%; <i>P</i> < 0.0001) and dysgeusia (53.3 versus 37.3%; <i>P</i> < 0.0001) more frequently than breakthrough infection patients. NNP breakthrough infection more frequently reported dizziness compared to NNP pre-vaccination infection patients (61.5 versus 50.6%; <i>P</i> = 0.001). Both PNP and NNP patients had impaired quality-of-life in cognitive, fatigue, sleep, anxiety and depression domains with no differences between pre-vaccination infection and breakthrough infection groups. PNP patients performed worse on National Institutes of Health Toolbox tests of processing speed, attention, executive function and working memory than a US normative population whereas NNP patients had lower results in processing, speed, attention and working memory, without differences between pre-vaccination infection and breakthrough infection groups. These results indicate that vaccination prior to SARS-CoV-2 infection does not affect the neurologic manifestations of long COVID in either PNP or NNP patients. Minor differences in neurologic symptoms between pre-vaccination infection and breakthrough infection groups may be caused by SARS-CoV-2 strains evolution. Patients developing Neuro-PASC after breakthrough infection have a higher burden of comorbidities, highlighting ","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcae448"},"PeriodicalIF":4.1,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11703551/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142960176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polygenic risk scores for atrial fibrillation and heart failure and the risk of stroke and dementia.","authors":"Lina Rydén, Nazib M Seidu, Hanna Wetterberg, Jenna Najar, Margda Waern, Silke Kern, Kaj Blennow, Henrik Zetterberg, Ingmar Skoog, Anna Zettergren","doi":"10.1093/braincomms/fcae477","DOIUrl":"10.1093/braincomms/fcae477","url":null,"abstract":"<p><p>Atrial fibrillation and heart failure have both been suggested to increase stroke and dementia risk. However, in observational studies, reversed causation and unmeasured confounding may occur. To mitigate these issues, this study aims to investigate if higher genetic risk for atrial fibrillation and heart failure increases dementia and stroke risk. Data were obtained from the population-based Gothenburg H70 Birth Cohort Studies in Sweden. Participants (<i>N</i> = 984) were born in 1930 with baseline examinations at age 70, 75, 79 or 85 and follow-ups until age 88-89. Polygenic risk scores at the 5 × 10^-8, 1 × 10^-5, 1 × 10^-3 and 1 × 10^-1 thresholds were generated for atrial fibrillation and heart failure. Stroke was diagnosed based on self-reports, close-informant interviews, and the National Patient Register. Dementia was diagnosed based on neuropsychiatric examinations, close-informant interviews, and the National Patient Register. Cox regression analyses were performed, adjusted for sex, age at baseline and the first five principal components to correct for population stratification. Those within the highest atrial fibrillation-polygenic risk score tertile had a 1.5 (95% CI 1.09-2.03) increased risk of dementia (at the 1 × 10^-5 threshold) and a 1.5 (95% CI 1.07-2.03) increased risk of stroke (at the 1 × 10^-3 threshold) compared to the lowest tertile. Those within the highest heart failure-polygenic risk score tertile had a 1.6 (95% CI 1.19-2.27) increased risk of dementia (at the 5 × 10^-8 threshold), but no increased risk of stroke (HR 1.2; 95% CI 0.83-1.60 at the 1 × 10^-5 threshold), compared to the lowest tertile. When analysing the polygenic risk scores as a continuous variable, the associations were in the same direction, although weaker. This study, investigating genetic risk of atrial fibrillation and heart failure in relation to stroke and dementia, supports the increasing body of evidence suggesting that atrial fibrillation is associated with both stroke and dementia risk. Whether heart failure increases dementia risk is less established, but the present study found that genetic risk of heart failure increased dementia risk. The finding that genetic risk for heart failure did not increase stroke risk needs to be interpreted with caution, as it may be due to a lack of statistical power. There are guidelines on how to best treat atrial fibrillation to prevent stroke, but more knowledge is needed on how to treat atrial fibrillation and heart failure to prevent dementia.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcae477"},"PeriodicalIF":4.1,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11748287/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143018297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction of: Causal relationship between multiparameter brain MRI phenotypes and age: evidence from Mendelian randomization.","authors":"","doi":"10.1093/braincomms/fcae461","DOIUrl":"https://doi.org/10.1093/braincomms/fcae461","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.1093/braincomms/fcae077.].</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcae461"},"PeriodicalIF":4.1,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11704780/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142960173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-omics characterization of improved cognitive functions in Parkinson's disease patients after the combined metabolic activator treatment: a randomized, double-blinded, placebo-controlled phase II trial.","authors":"Burak Yulug, Ozlem Altay, Xiangyu Li, Lutfu Hanoglu, Seyda Cankaya, Halil A Velioglu, Simon Lam, Hong Yang, Ebru Coskun, Ezgi Idil, Zubeyir Bayraktaroglu, Rahim Nogaylar, Ahmet Ozsimsek, Serkan Yildirim, Ismail Bolat, Metin Kiliclioglu, Cemil Bayram, Nursena Yuksel, Ozlem O Tozlu, Muhammad Arif, Saeed Shoaie, Ahmet Hacimuftuoglu, Cheng Zhang, Jens Nielsen, Hasan Turkez, Jan Borén, Mathias Uhlén, Adil Mardinoglu","doi":"10.1093/braincomms/fcae478","DOIUrl":"10.1093/braincomms/fcae478","url":null,"abstract":"<p><p>Parkinson's disease is primarily marked by mitochondrial dysfunction and metabolic abnormalities. We recently reported that the combined metabolic activators improved the immunohistochemical parameters and behavioural functions in Parkinson's disease and Alzheimer's disease animal models and the cognitive functions in Alzheimer's disease patients. These metabolic activators serve as the precursors of nicotinamide adenine dinucleotide and glutathione, and they can be used to activate mitochondrial metabolism and eventually treat mitochondrial dysfunction. Here, we designed a randomized, double-blinded, placebo-controlled phase II study in Parkinson's disease patients with 84 days combined metabolic activator administration. A single dose of combined metabolic activator contains L-serine (12.35 g), <i>N</i>-acetyl-L-cysteine (2.55 g), nicotinamide riboside (1 g) and L-carnitine tartrate (3.73 g). Patients were administered either one dose of combined metabolic activator or a placebo daily for the initial 28 days, followed by twice-daily dosing for the next 56 days. The main goal of the study was to evaluate the clinical impact on motor functions using the Unified Parkinson's Disease Rating Scale and to determine the safety and tolerability of combined metabolic activator. A secondary objective was to assess cognitive functions utilizing the Montreal Cognitive Assessment and to analyse brain activity through functional MRI. We also performed comprehensive plasma metabolomics and proteomics analysis for detailed characterization of Parkinson's disease patients who participated in the study. Although no improvement in motor functions was observed, cognitive function was shown to be significantly improved (<i>P</i> < 0.0000) in Parkinson's disease patients treated with the combined metabolic activator group over 84 days, whereas no such improvement was noted in the placebo group (<i>P</i> > 0.05). Moreover, a significant reduction (<i>P</i> = 0.001) in Montreal Cognitive Assessment scores was observed in the combined metabolic activator group, with no decline (<i>P</i> > 0.05) in the placebo group among severe Parkinson's disease patients with lower baseline Montreal Cognitive Assessment scores. We showed that improvement in cognition was associated with critical brain network alterations based on functional MRI analysis, especially relevant to areas with cognitive functions in the brain. Finally, through a comprehensive multi-omics analysis, we elucidated the molecular mechanisms underlying cognitive improvements observed in Parkinson's disease patients. Our results show that combined metabolic activator administration leads to enhanced cognitive function and improved metabolic health in Parkinson's disease patients as recently shown in Alzheimer's disease patients. The trial was registered in ClinicalTrials.gov NCT04044131 (17 July 2019, https://clinicaltrials.gov/ct2/show/NCT04044131).</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcae478"},"PeriodicalIF":4.1,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11733689/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143018231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-motor asymmetry and dopamine degeneration in Parkinson's disease.","authors":"Frederik O Hansen, Karoline Knudsen, Malene F Damholdt, Toke Bek, Per Borghammer, Niels Okkels","doi":"10.1093/braincomms/fcaf002","DOIUrl":"10.1093/braincomms/fcaf002","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Asymmetric dopaminergic degeneration of the striatum is a characteristic feature of Parkinson's disease, associated with right-left asymmetry in motor function. As such, studying asymmetry provides insights into progressive neurodegeneration between cerebral hemispheres. Given the impact of Lewy pathology on various neurotransmitter systems beyond the dopaminergic, it may be that other neuronal systems in the predominantly affected hemisphere are similarly affected. According to this hypothesis, asymmetry in dopaminergic degeneration would be expected to coincide with asymmetry in other neurotransmitter systems. Consequently, asymmetry in functions primarily dependent on dopaminergic integrity, such as motor function, should correlate with asymmetry in bilateral non-motor functions that rely on other cerebral systems, such as pupillary function. Therefore, this study tested whether right-left asymmetry in bilateral non-motor measures correlates with asymmetry in dopaminergic striatal integrity. We also tested whether asymmetric striatal degeneration is associated with greater asymmetry in non-motor measures overall. Using a comparative cross-sectional design, we recruited newly diagnosed patients with Parkinson's disease with predominantly right-sided (&lt;i&gt;n&lt;/i&gt; = 18), left-sided (&lt;i&gt;n&lt;/i&gt; = 15) or symmetric nigrostriatal denervation (&lt;i&gt;n&lt;/i&gt; = 15) assessed on dopamine PET. Detailed examinations of lateralized non-motor function included lacrimation, hand skin wrinkling, salivation, olfaction and pupillary function. Healthy controls were recruited for comparison. We observed a moderate-to-strong correlation between right-left asymmetry of putamen dopamine binding and asymmetry in pupillary redilation speed [Spearman's rank correlation coefficient (&lt;i&gt;r&lt;sub&gt;s&lt;/sub&gt;&lt;/i&gt; ) = -0.53, 95% confidence interval (-0.77; -0.14), &lt;i&gt;P&lt;/i&gt; = 0.0084]. We also observed moderate correlations between non-negative putaminal asymmetry and lacrimation [&lt;i&gt;r&lt;sub&gt;s&lt;/sub&gt;&lt;/i&gt; = 0.35, (-0.00; 0.62), &lt;i&gt;P&lt;/i&gt; = 0.0464] and word recognition [&lt;i&gt;r&lt;sub&gt;s&lt;/sub&gt;&lt;/i&gt; = 0.36, (0.01; 0.63), &lt;i&gt;P&lt;/i&gt; = 0.0410]. However, none were significant after false discovery rate correction. We observed significant group differences in non-negative asymmetry in salivation (&lt;i&gt;P&lt;/i&gt; = 0.0390, ANOVA) and a trend towards greater asymmetric lacrimation in participants with asymmetric striatal dopamine loss compared with healthy controls (&lt;i&gt;P&lt;/i&gt; = 0.0330, unadjusted). Additionally, participants with asymmetric striatal dopaminergic binding showed greater, though non-significant, asymmetry in all pupillary measures compared with those with symmetric dopaminergic binding. In conclusion, this study contributes to our understanding of neurodegeneration progression in Parkinson's disease and suggests a link between dopaminergic degeneration and non-motor measures related to autonomic function, particularly salivation, lacrimation and pupillary function. While our findings do not support a stri","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcaf002"},"PeriodicalIF":4.1,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11752486/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143025830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The <i>FGF14</i> GAA repeat expansion is a major cause of ataxia in the Cypriot population.","authors":"Ioannis Livanos, Christina Votsi, Kyriaki Michailidou, David Pellerin, Bernard Brais, Stephan Zuchner, Marios Pantzaris, Kleopas A Kleopa, Eleni Zamba Papanicolaou, Kyproula Christodoulou","doi":"10.1093/braincomms/fcae479","DOIUrl":"10.1093/braincomms/fcae479","url":null,"abstract":"<p><p>Dominantly inherited intronic GAA repeat expansions in the fibroblast growth factor 14 gene have recently been shown to cause spinocerebellar ataxia 27B. Currently, the pathogenic threshold of (GAA)_≥300 repeat units is considered highly penetrant, while (GAA)_250-299 is likely pathogenic with reduced penetrance. This study investigated the frequency of the GAA repeat expansion and the phenotypic profile in a Cypriot cohort with unresolved late-onset cerebellar ataxia. We analysed this trinucleotide repeat in 155 patients with late-onset cerebellar ataxia and 227 non-neurological disease controls. The repeat locus was examined by long-range PCR followed by fragment analysis using capillary electrophoresis, agarose gel electrophoresis and automated electrophoresis. A comprehensive comparison of all three electrophoresis techniques was conducted. Additionally, bidirectional repeat-primed PCRs and Sanger sequencing were carried out to confirm the absence of any interruptions or non-GAA motifs in the expanded alleles. The (GAA)_≥250 repeat expansion was present in 12 (7.7%) patients. The average age at disease onset was 60 ± 13.5 years. The earliest age of onset was observed in a patient with a (GAA)₂₈₇ repeat expansion, with ataxia symptoms appearing at 25 years of age. All patients with spinocerebellar ataxia 27B displayed symptoms of gait and appendicular ataxia. Nystagmus was observed in 41.7% of the patients, while 58.3% exhibited dysarthria. Our findings indicate that spinocerebellar ataxia 27B represents the predominant aetiology of autosomal dominant cerebellar ataxia in the Cypriot population, as this is the first dominant repeat expansion ataxia type detected in this population. Given our results and existing research, we propose including fibroblast growth factor 14 GAA repeat expansion testing as a first-tier genetic diagnostic approach for patients with late-onset cerebellar ataxia.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcae479"},"PeriodicalIF":4.1,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11724429/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142973632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cochlear implantation in adults with acquired single-sided deafness improves cortical processing and comprehension of speech presented to the non-implanted ears: a longitudinal EEG study.","authors":"Ya-Ping Chen, Patrick Neff, Sabine Leske, Daniel D E Wong, Nicole Peter, Jonas Obleser, Tobias Kleinjung, Andrew Dimitrijevic, Sarang S Dalal, Nathan Weisz","doi":"10.1093/braincomms/fcaf001","DOIUrl":"10.1093/braincomms/fcaf001","url":null,"abstract":"<p><p>Former studies have established that individuals with a cochlear implant (CI) for treating single-sided deafness experience improved speech processing after implantation. However, it is not clear how each ear contributes separately to improve speech perception over time at the behavioural and neural level. In this longitudinal EEG study with four different time points, we measured neural activity in response to various temporally and spectrally degraded spoken words presented monaurally to the CI and non-CI ears (5 left and 5 right ears) in 10 single-sided CI users and 10 age- and sex-matched individuals with normal hearing. Subjective comprehension ratings for each word were also recorded. Data from single-sided CI participants were collected pre-CI implantation, and at 3, 6 and 12 months after implantation. We conducted a time-resolved representational similarity analysis on the EEG data to quantify whether and how neural patterns became more similar to those of normal hearing individuals. At 6 months after implantation, the speech comprehension ratings for the degraded words improved in both ears. Notably, the improvement was more pronounced for the non-CI ears than the CI ears. Furthermore, the enhancement in the non-CI ears was paralleled by increased similarity to neural representational patterns of the normal hearing control group. The maximum of this effect coincided with peak decoding accuracy for spoken-word comprehension (600-1200 ms after stimulus onset). The present data demonstrate that cortical processing gradually normalizes within months after CI implantation for speech presented to the non-CI ear. CI enables the deaf ear to provide afferent input, which, according to our results, complements the input of the non-CI ear, gradually improving its function. These novel findings underscore the feasibility of tracking neural recovery after auditory input restoration using advanced multivariate analysis methods, such as representational similarity analysis.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcaf001"},"PeriodicalIF":4.1,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11733687/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dissociable components of visual perceptual learning characterized by non-invasive brain stimulation: Stage 1 Registered Report.","authors":"Marcello Maniglia","doi":"10.1093/braincomms/fcae468","DOIUrl":"10.1093/braincomms/fcae468","url":null,"abstract":"<p><p>Visual perceptual learning (VPL), the training-induced improvement in visual tasks, has long been considered the product of neural plasticity at early and local stages of signal processing. However, recent evidence suggests that multiple networks and mechanisms, including stimulus- and task-specific plasticity, concur in generating VPL. Accordingly, early models of VPL, which characterized learning as being local and mostly involving early sensory areas, such as V1, have been updated to embrace these newfound complexities, acknowledging the involvement on parietal (i.e. intra-parietal sulcus) and frontal (i.e. dorsolateral prefrontal cortex) areas, in aspects concerning decision-making, feedback integration and task structure. However, evidence of multiple brain regions differentially involved in different aspects of learning is thus far mostly correlational, emerging from electrophysiological and neuroimaging techniques. To directly address these multiple components of VPL, we propose to use a causal neuromodulation technique, namely transcranial random noise stimulation, to selectively modulate the activity of different brain regions suggested to be involved in various aspects of learning. Specifically, we will target a region in the occipital cortex, which has been associated with stimulus-specific plasticity, and one in the parietal cortex, which has been associated with task-specific plasticity, in a between-subject design. Measures of transfer of learning to untrained stimuli and tasks will be used to evaluate the role of different regions and test for double dissociations between learning effects and stimulated area, shedding lights on learning mechanisms in the visual system. Evidence of dissociable mechanisms of learning can help refine current models of VPL and may help develop more effective visual training and rehabilitation protocols.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcae468"},"PeriodicalIF":4.1,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11694700/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142924203","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of diet and ovariectomy on <i>Toxoplasma gondii</i> brain infection: functional alterations and neuronal loss in rats.","authors":"Nene Ahidjo, Paul F Seke Etet, Leonard Ngarka, Frederic Maidawa Yaya, Ethel W Ndianteng, Aude L Eyenga Nna, Luc Yvan Meka'a Zang, Christelle Kemmo, Caroline N C Nwasike, Floriane G Yonkeu Tatchou, Wepnyu Y Njamnshi, Leonard N Nfor, Patrick V Tsouh Fokou, Sefirin Djiogue, Fabrice Fekam Boyom, Bonaventure T Ngadjui, Alfred K Njamnshi","doi":"10.1093/braincomms/fcae441","DOIUrl":"10.1093/braincomms/fcae441","url":null,"abstract":"<p><p>Epidemiological evidence associates <i>Toxoplasma gondii</i> latent infection with the development of neuropsychiatric disorders, and various immunological and environmental factors play key pathophysiological roles through host immune response alterations. We investigated the cognitive and motor alterations occurring in the terminal stage of <i>T. gondii</i> infection in rats, and whether a low-protein diet, a high-fat diet or ovariectomy may accelerate their development, given the role of malnutrition and menopause on immunity and resistance to infection. In two sets of experiments, 2-month-old (157.5 ± 4.3 g, <i>n</i> = 42) male (<i>n</i> = 18) and female (<i>n</i> = 24) Wistar rats were infected with <i>T. gondii</i> (ATCC 40050). Open-field and elevated plus maze tests were performed in the terminal stage of infection first and then in the early stage in low-protein diet-fed, high-fat diet-fed and ovariectomized infected rats. Late-stage (90 days) infected and early-stage (17 days) low-protein diet-fed groups showed significant decreases in body weight (42.42%↓, <i>P</i> = 0.016 and 57.14%↓, <i>P</i> < 0.001 versus non-infected, respectively), increases in body temperature (<i>P</i> = 0.001 and <i>P</i> < 0.001, respectively), decreases in blood glucose levels (<i>P</i> = 0.006 and <i>P</i> = 0.020, respectively), signs of cognitive and motor impairment and lower neuron counts. The alterations observed in high-fat diet-fed and ovariectomized infected animals were milder. Low-protein diet feeding to <i>T. gondii</i>-infected rats accelerated the occurrence of the infection terminal stage. Thus, a diet low in proteins could transform a slow early-stage <i>T. gondii</i> infection into an active neurotoxoplasmosis with neuropsychiatric manifestations and possible neurodegeneration in rats.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcae441"},"PeriodicalIF":4.1,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11686407/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142916571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aberrant functional connectivity between the retrosplenial cortex and hippocampal subregions in amnestic mild cognitive impairment and Alzheimer's disease.","authors":"Junkai Wang, Shui Liu, Peipeng Liang, Bin Cui, Zhiqun Wang","doi":"10.1093/braincomms/fcae476","DOIUrl":"10.1093/braincomms/fcae476","url":null,"abstract":"&lt;p&gt;&lt;p&gt;The posterior cingulate cortex and hippocampus are the core regions involved in episodic memory, and they exhibit functional connectivity changes in the development and progression of Alzheimer's disease. Previous studies have demonstrated that the posterior cingulate cortex and hippocampus are both cytoarchitectonically heterogeneous regions. Specifically, the retrosplenial cortex, typically subsumed under the posterior cingulate cortex, is an area functionally and anatomically distinct from the posterior cingulate cortex, and the hippocampus is composed of several subregions that participate in multiple cognitive processes. However, little is known about the functional connectivity patterns of the retrosplenial cortex or other parts of the posterior cingulate cortex with hippocampal subregions and their differential vulnerability to Alzheimer's disease pathology. Demographic data, neuropsychological assessments, and resting-state functional magnetic resonance imaging data were collected from 60 Alzheimer's disease participants, 60 participants with amnestic mild cognitive impairment, and 60 sex-matched normal controls. The bilateral retrosplenial cortex, other parts of the posterior cingulate cortex, and hippocampus subregions (including the bilateral anterior hippocampus and posterior hippocampus) were selected to investigate functional connectivity alterations in amnestic mild cognitive impairment and Alzheimer's disease. Resting-state functional connectivity analysis demonstrated heterogeneity in the degree of connectivity between the hippocampus and different parts of the total posterior cingulate cortex, with considerably greater functional connectivity of the retrosplenial cortex with the hippocampus compared with other parts of the posterior cingulate cortex. Furthermore, the bilateral retrosplenial cortex exhibited widespread intrinsic functional connectivity with all anterior-posterior hippocampus subregions. Compared to the normal controls, the amnestic mild cognitive impairment and Alzheimer's disease groups showed different magnitudes of decreased functional connectivity between the retrosplenial cortex and the contralateral posterior hippocampus. Additionally, diminished functional connectivity between the left retrosplenial cortex and right posterior hippocampus was correlated with clinical disease severity in amnestic mild cognitive impairment subjects, and the combination of multiple functional connectivity indicators of the retrosplenial cortex can discriminate the three groups from each other. These findings confirm and extend previous studies suggesting that the retrosplenial cortex is extensively and functionally connected with hippocampus subregions and that these functional connections are selectively affected in the Alzheimer's disease continuum, with prominent disruptions in functional connectivity between the retrosplenial cortex and contralateral posterior hippocampus underpinning episodic memory impairment assoc","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcae476"},"PeriodicalIF":4.1,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11733685/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}