Journal of chemical neuroanatomy最新文献

{"title":"Neuroprotective anticonvulsant and anxiolytic effects of octreotide in wistar rats","authors":"Tahereh Karimi Shayan ,&nbsp;Arash Abdolmaleki ,&nbsp;Asadollah Asadi ,&nbsp;Hossein Hassanpour","doi":"10.1016/j.jchemneu.2023.102320","DOIUrl":"10.1016/j.jchemneu.2023.102320","url":null,"abstract":"<div><p>Somatostatin<span><span><span> interneurons<span> exhibited anti-epileptic activity. As a result, somatostatin agonists appear to be a promising target for antiepileptic drug development (AEDs). In this regard, we investigated the effects of octreotide<span>, a somatostatin analog, on </span></span></span>pentylenetetrazol<span> (PTZ)-induced seizures in male Wistar rats<span><span><span>. Animals were given octreotide at doses of 50 or 100 µg/kg for seven days. The anxiolytic effects of octreotide were then evaluated using open field and elevated plus-maze tests. Following that, mice were intraperitoneally given a single convulsive dosage of PTZ (60 mg/kg) and then monitored for 30 min for symptoms of seizures. Finally, the antioxidant capacity of brain tissue and histopathological changes in the hippocampus were investigated. Octreotide therapy for seven days at 50 or 100 µg/kg was more effective than </span>diazepam in preventing acute PTZ-induced seizures (P &lt; 0.05). Furthermore, both octreotide dosages revealed substantial anxiolytic effects in open-field and elevated plus-maze tests compared to untreated rats. Nonetheless, octreotide's anxiolytic impact was less effective than diazepam's. On the other hand, octreotide also suppressed </span>neuronal apoptosis and attenuated </span></span></span>oxidative stress<span>. Our results suggest that chronic administration of octreotide has anticonvulsant, anxiolytic, and antioxidant activity in the male Wistar rat model.</span></span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102320"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10281403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroprotective effect of quercetin nanoparticles: A possible prophylactic effect in cerebellar neurodegenerative disorders","authors":"Nashwa Fathy Gamal El-Tahawy ,&nbsp;Rehab Ahmed Rifaai ,&nbsp;Entesar Ali Saber ,&nbsp;Seham A.Abd El-Aleem ,&nbsp;Hanaa Hassanein Mohammed","doi":"10.1016/j.jchemneu.2023.102307","DOIUrl":"10.1016/j.jchemneu.2023.102307","url":null,"abstract":"<div><p><span><span><span>Memory deficit, anxiety, coordination deficit and depression are common neurological disorders<span> attributed to aluminum (Al) buildup in the nervous system. </span></span>Quercetin nanoparticles (QNPs) are a newly developed effective neuroprotectant. We aimed to investigate the potential protective and therapeutic effects of QNPs in Al induced toxicity in rat </span>cerebellum. A rat model of Al-induced cerebellar damage was created by AlCl</span>₃ (100 mg/kg) administration orally for 42 days. QNPs (30 mg/kg) was administered for 42-days as a prophylactic (along with AlCl₃ administration) or therapeutic for 42-days (following AlCl₃<span><span> induced cerebellar damage). Cerebellar tissues were assessed for structural and molecular changes. The results showed that Al induced profound cerebellar structural and molecular changes, including neuronal damage, astrogliosis and </span>tyrosine hydroxylase<span> downregulation. Prophylactic QNPs significantly reduced Al induced cerebellar neuronal degeneration<span>. QNPs is a promising neuroprotectant that can be used in elderly and vulnerable subjects to protect against neurological deterioration. It could be a promising new line for therapeutic intervention in neurodegenerative diseases.</span></span></span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102307"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10279544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-inflammatory, anticholinesterase, antioxidant, and memory enhancement potential of Phyllanthus amarus in potassium-dichromate induced neurotoxicity of male Wistar rats","authors":"Kingsley Afoke Iteire ,&nbsp;Tolulope Judah Gbayisomore ,&nbsp;Olalekan Marvelous Olatuyi","doi":"10.1016/j.jchemneu.2023.102308","DOIUrl":"10.1016/j.jchemneu.2023.102308","url":null,"abstract":"<div><p>This study investigated the protective effect of aqueous <span><em>Phyllanthus amarus</em></span><span><span><span> leaf extract (APALE) in Potassium dichromate<span> (PDc)-induced neurotoxicity. Seventy young adult male, </span></span>Wistar rats with a weight of 130–150 g, were randomised into seven groups (n = 10): Group 1; distilled water; Group 2: 300 mg/kg APALE; Group 3: 17 mg/kg PDc; Group 4: 5 mg/kg </span>Donepezil<span><span><span> (DPZ); Group 5: 17 mg/kg PDc + 400 mg/kg APALE; Group 6:17 mg/kg PDc + 200 mg/kg APALE; Group 7: 17 mg/kg PDc + 5 mg/kg DPZ. All administrations were given once daily via an orogastric cannula for 28 consecutive days. Cognitive assessment tests were employed to ascertain the treatments' effects on the rats' cognitive function. At the end of the experiment, the rats were sacrificed, morphometric analysis was done, and the brains were dissected for histology, enzyme, and other </span>biochemical analysis<span><span>. Findings from this study showed that APALE significantly improved locomotive activity, recognition memory sensitivity, protection against fear and anxiety, enhanced decision-making, and improved memory function in a dose-dependent manner comparably to DPZ. In addition, APALE significantly increased antioxidants level, reducing oxidative stress in PDc-induced neurotoxic rats and significantly reducing brain </span>acetylcholinesterase (AchE) activity by regulating </span></span>gamma amino butyric acid (GABA) levels in PDc-induced neurotoxic rats compared to DPZ. Furthermore, APALE alleviated neuroinflammatory responses via maintaining histoarchitecture and down-regulation of IBA1 and Tau in PDc-induced rats. In conclusion, APALE protected against PDc-induced neurotoxicity via a combination of anti-inflammatory, anticholinergic, and antioxidant effects on the prefrontal cortex of rats.</span></span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102308"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10332710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Changes in hypothalamic mu-opioid receptor expression following acute olanzapine treatment in female rats: Implications for feeding behavior","authors":"Maiken Krogsbaek ,&nbsp;Nick Yao Larsen ,&nbsp;Anne M. Landau ,&nbsp;Connie Sanchez ,&nbsp;Jens Randel Nyengaard","doi":"10.1016/j.jchemneu.2023.102324","DOIUrl":"10.1016/j.jchemneu.2023.102324","url":null,"abstract":"<div><p>Advances have been made in recent years in using opioid receptor antagonists as an adjunct therapy to psychotropic medication to reduce debilitating weight gain and metabolic adverse effects associated with in particular second generation antipsychotics. However, it is unknown whether second generation antipsychotics produce a change in opioid receptor expression in the brain. The present study investigated early changes in opioid receptor expression in the female rat hypothalamus, a master controller of hunger and metabolic regulation, after acute treatment with olanzapine, a commonly used second generation antipsychotic. Using quantitative spatial in situ hybridization and receptor autoradiography, expression levels of the three opioid receptors; kappa, mu and delta, were determined at mRNA and protein level, respectively, in the five hypothalamic areas: paraventricular nucleus, arcuate nucleus, ventromedial nucleus, dorsomedial nucleus and lateral hypothalamus. After 48 h of olanzapine treatment at clinically relevant plasma concentration weight gain and food intake changes, and increased plasma glucose were observed in female rats. Olanzapine treatment also led to a significant increase in mu opioid receptor availability in the arcuate nucleus, which contains both satiety and hunger controlling neurons. No other areas showed any opioid receptor expressional changes with olanzapine treatment on neither at mRNA nor protein level. Technical difficulties made it impossible to analyze mRNA levels in the lateral hypothalamus and overall binding of delta opioid receptors. Thus, the present study provided insights in to how olanzapine at clinically relevant plasma levels already at an early stage modulated the opioid system in the hypothalamus.</p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102324"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10647452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Application of the wholebrain calculation interactive framework to map whole-brain neural connectivity networks","authors":"Liping Ma,&nbsp;He Liu,&nbsp;Ziyi Xu,&nbsp;Mengli Yang,&nbsp;Yinghua Zhang","doi":"10.1016/j.jchemneu.2023.102304","DOIUrl":"10.1016/j.jchemneu.2023.102304","url":null,"abstract":"<div><p>The aim of this work was <strong>t</strong><span><span><span>o develop a simple and feasible method of mapping the neural network<span> topology of the mouse brain. Wild-type C57BL/6 J mice (n = 10) aged 8–10 weeks were injected with the cholera toxin subunit B (CTB) tracer in the anterior (NAcCA) and posterior (NAcCP) parts of the nucleus accumbens (NAc) core and in the medial (NAcSM) and lateral (NAcSL) parts of the </span></span>NAc shell. The labeled neurons were reconstructed using the WholeBrain Calculation Interactive Framework. The NAcCA receives neuronal projections from the olfactory areas (OLF) and </span>isocortex<span><span>; the thalamus and isocortex project more fibers to the NAcSL, and the hypothalamus send more fiber projections to the </span>NAcSM. Cell resolution can be automatically annotated, analyzed, and visualized using the WholeBrain Calculation Interactive Framework, making large-scale mapping of mouse brains at cellular and subcellular resolutions easier and more accurate.</span></span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102304"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10272286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Isoflurane-induced reduction in neurogenesis derived from the tertiary dentate matrix","authors":"Xin-Li Xiao ,&nbsp;Da-Meng Pan ,&nbsp;Zhe-Qian Zhang ,&nbsp;Tao Wang ,&nbsp;Ding-Hui Li ,&nbsp;Chu-Tong Zhang ,&nbsp;Le-Fan Liu ,&nbsp;Yu Chen ,&nbsp;Shu-Nan Yang ,&nbsp;Jing Tan ,&nbsp;Guan-Ling Fu ,&nbsp;Yan-Bing Ma ,&nbsp;Xiao-Lin Wu ,&nbsp;Jin-Song Zhou ,&nbsp;Feng Wu ,&nbsp;Kai-Wei Si ,&nbsp;Jian-Xin Liu","doi":"10.1016/j.jchemneu.2023.102325","DOIUrl":"10.1016/j.jchemneu.2023.102325","url":null,"abstract":"<div><p><span><span>Anesthetics-induced disruption of dentate neurogenesis in the young brain is strongly suggested to contribute to delayed neurocognitive deficit. In postnatal rodents, the neurogenesis of the </span>dentate gyrus<span><span><span><span> (DG) is sequentially derived from the secondary dentate matrix, tertiary dentate matrix and subgranular zone (SGZ). However, the effects of anesthetics on the dentate neurogenesis derived from specific sites are poorly understood. To trace the new cells generated from the postnatal secondary dentate matrix, peak stage of the tertiary dentate matrix and early stage of the SGZ after isoflurane exposure, mice at postnatal day 1 (P1), P7 and P31 were injected with BrdU at 12 h before the exposure. We found that isoflurane exposure significantly reduced the numbers of </span>proliferating cells (1 day old), immature </span>granule cells (21 days old) or mature granule cells (42 days old) derived from the peak stage of the tertiary dentate matrix and postnatal secondary dentate matrix, but not from the SGZ. </span>Quantitative assessment<span> of BrdU-/BrdU+NeuN-positive cells and cleaved caspase-3 level in the DG indicated that the reduction was correlated with cell loss rather than neuronal differentiation. Mechanistically, we demonstrated that the PI3K/Akt/GSK-3β pathway enriched by mRNA-sequencing is a requirement for the isoflurane-induced loss of 1-day-old proliferating cells generated from the tertiary dentate matrix. In addition, this study demonstrated that P1 and P7 mice, but not P31 mice exposure to isoflurane resulted in subsequent deficits in performance of the tasks of the Morris </span></span></span>Water Maze.</p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102325"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10274803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Thimet oligopeptidase (THOP 1) distribution in cane toad (Bufo Marinus, Linnaeus, 1758) brain","authors":"Diogo M.L.P. Cavalcanti ,&nbsp;Tiago S. Teófilo ,&nbsp;Tayline D. Rodrigues ,&nbsp;Tayssa N.S. Barbosa ,&nbsp;José D. Fontenele-Neto","doi":"10.1016/j.jchemneu.2023.102345","DOIUrl":"10.1016/j.jchemneu.2023.102345","url":null,"abstract":"<div><p><span><span>Thimet oligopeptides (THOP 1) is a metal-dependent </span>peptidase<span><span> involved in the metabolism of neuropeptides and the presentation of peptides via MHC-1. It has been shown to play a role in the regulation of protein-protein interactions and the metabolism of intracellular peptides. THOP 1 is associated with important </span>biological processes<span> such as metabolism and neurodegenerative diseases, among others. The objective of this study is to elucidate the distribution of THOP 1 in the </span></span></span><span><em>Bufo marinus</em></span><span> brain. The analysis of THOP 1 amino acid sequences<span> indicates that they have been conserved throughout evolution, with significant homology observed across various phyla. When comparing amphibians with other species, more than 70% identity can be identified. Immunohistochemistry<span> analysis of the toad's brain has demonstrated that the enzyme has a ubiquitous distribution, consistent with previous findings in mammals. THOP 1 can be found in important areas of the brain, such as bulb, thalamic nuclei, striatum, hypothalamus, and among others. Nonetheless, THOP 1 is consistently localized within the nucleus, a pattern also observed in the rat brain. Therefore, based on these results, the toad appears to be an excellent model for studying the general biology of THOP 1, given the substantial homology of this enzyme with mammals and its similarity in distribution within the brain.</span></span></span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"133 ","pages":"Article 102345"},"PeriodicalIF":2.8,"publicationDate":"2023-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41130712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Localization and neurochemical identity of alpha1-adrenergic receptor-containing elements in the mouse locus coeruleus","authors":"Zachary N.M. Luyo ,&nbsp;Abigail B. Lawrence ,&nbsp;Theodore G. Stathopoulos ,&nbsp;Darlene A. Mitrano","doi":"10.1016/j.jchemneu.2023.102343","DOIUrl":"10.1016/j.jchemneu.2023.102343","url":null,"abstract":"<div><p><span>The locus coeruleus<span> (LC) is the major source for norepinephrine<span> (NE) in the brain and projects to areas involved in learning and memory, reward, arousal, attention, and autonomic functions related to stress. There are three types of adrenergic receptors<span> that respond to NE: alpha1-, alpha2-, and beta-adrenergic receptors. Previous behavioral studies have shown the alpha1-adrenergic receptor (α1AR) to be present in the LC, however, with conflicting results. For example, it was shown that α1ARs in the LC are involved in some of the motivational effects of stimulation of the medial forebrain bundle<span><span>, which was reduced by α1AR antagonist terazosin. Another study showed that during novelty-induced behavioral activation, the α1AR antagonist </span>prazosin reduced c-fos expression in brain regions known to contain motoric α1ARs, except for the LC, where c-fos expression was enhanced. Despite new research delineating more specific connectivity of the neurons in the LC, and some roles of the adrenergic receptors, the α1ARs have not been localized at the subcellular level. Therefore, in order to gain a greater understanding of the aforementioned studies, we used </span></span></span></span></span>immunohistochemistry<span> at the electron microscopic (EM) level to determine which neuronal or glial elements in the LC express the α1AR. We hypothesized, based on previous work in the ventral periaqueductal gray<span> area, that the α1AR would be found mainly presynaptically in axon terminals<span><span>, and possibly in glial elements. Single labeling immunohistochemistry at the EM revealed that about 40% of labeled elements that contained the α1AR were glial elements, while approximately 50% of the labeled neuronal elements were axon terminals or small unmyelinated axons in the LC. Double labeling immunohistochemistry found the α1AR expressed in GFAP-labeled astrocytes, in both GABAergic and glutamatergic axon terminals, and in a portion of the α1AR dendrites, colocalized with </span>tyrosine hydroxylase (TH, a marker for noradrenergic neurons). This study sheds light on the neuroanatomical framework underlying the effects of NE and pharmaceuticals acting directly or indirectly on α1ARs in the LC.</span></span></span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"133 ","pages":"Article 102343"},"PeriodicalIF":2.8,"publicationDate":"2023-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41101709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Celecoxib attenuates neuroinflammation, reactive astrogliosis and promotes neuroprotection in young rats with experimental hydrocephalus","authors":"Maurício Dutra ,&nbsp;Stephanya Covas da Silva ,&nbsp;Pâmella da Silva Beggiora Marques ,&nbsp;Izadora Oliveira Amaral ,&nbsp;Stephanie Naomi Funo de Souza ,&nbsp;Luiz Antônio Dutra ,&nbsp;Marcelo Volpon Santos ,&nbsp;Hélio Rubens Machado ,&nbsp;Luiza da Silva Lopes","doi":"10.1016/j.jchemneu.2023.102344","DOIUrl":"10.1016/j.jchemneu.2023.102344","url":null,"abstract":"<div><p><span>Hydrocephalus<span> is a neurological condition with altered cerebrospinal fluid flow<span> (CSF). The treatment is surgical and the most commonly used procedure is ventricle-peritoneal shunt. However, not all patients can undergo immediate surgery or achieve complete lesion reversal. Neuroprotective measures are valuable in such cases. It was evaluated whether the use of </span></span></span>celecoxib<span><span>, a selective inhibitor of COX-2, associated or not with ventricular-subcutaneous derivation, could offer benefits to the brain structures affected by experimental hydrocephalus. Seven-day-old male Wistar Hannover rats induced by intracisternal injection of kaolin 15% were used, divided into five groups with ten animals each: intact control (C), untreated hydrocephalus (H), hydrocephalus treated with celecoxib 20 mg/kg intraperitoneal (HTC), hydrocephalus treated with shunt (HTS) and hydrocephalus treated with shunt and celecoxib 20 mg/kg intraperitoneal (HTCS). Celecoxib was administered for 21 consecutive days, starting the day after hydrocephalus induction and continuing until the end of the experimental period. The surgery was performed seven days after inducing hydrocephalus. Multiple assessment methods were used, such as behavioral tests (water maze and open field), histological analysis (hematoxylin and eosin), </span>immunohistochemistry<span><span> (caspase-3, COX-2, and GFAP), and ELISA<span> analysis of GFAP. The results of the behavioral and memory tests indicated that celecoxib improves the neurobehavioral response. The improvement can be attributed to the reduced neuroinflammation (p &lt; 0.05), and </span></span>astrogliosis (p &lt; 0.05) in different brain regions. In conclusion, the results suggest that celecoxib holds great potential as an adjuvant neuroprotective drug for the treatment of experimental hydrocephalus.</span></span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"133 ","pages":"Article 102344"},"PeriodicalIF":2.8,"publicationDate":"2023-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41132263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurobiological and pathophysiological concepts of Christfried Jakob (1866–1956) on language and aphasia: An English translation of two communications [1910,1932] and a modern perspective","authors":"Maria E. Vasilopoulou ,&nbsp;Lazaros C. Triarhou","doi":"10.1016/j.jchemneu.2023.102341","DOIUrl":"10.1016/j.jchemneu.2023.102341","url":null,"abstract":"<div><p><span>The aim of the present article is to preserve, in English translation, two historical communications on aphasia and the pathophysiology of language by the neurobiologist Christfried Jakob (1866–1956) of Buenos Aires, and to place them in a modern perspective. The morphofunctional basis of human language and its pathology occupied Jakob’s mind over three decades. His synthetic conclusions were based on the neuropathological examination of dozens of aphasic cases from the Hospital de Las Mercedes and the National Women’s Psychiatric Hospital between 1906 and 1936. Special mention is made of the role of the </span>cerebellum<span><span>, the thalamus, and their connections with the </span>cerebral cortex, and the language network. Current research and imaging studies support and elaborate that which Jacob presented so many years ago; many of his analyses and ideas are informative and remain relevant today.</span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"133 ","pages":"Article 102341"},"PeriodicalIF":2.8,"publicationDate":"2023-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10286434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}