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Takahata, K.

Publications and source records attributed to Takahata, K..

13 recordsLinked to original sources

Postmortem Alterations of Metabotropic Glutamate Receptors across Neuropsychiatric Disorders: A Systematic Review

Metabotropic glutamate receptors (mGluRs) regulate glutamatergic transmission and have been implicated in diverse neuropsychiatric disorders, but human postmortem evidence remains fragmented. We aimed to map these findings across diagnoses, receptor subtypes, brain regions, and measurement modalities. Following PRISMA guidelines, we systematically searched MEDLINE, EMBASE, and Web of Science from inception to August 8, 2026, for studies assessing GRM transcripts, as well as mGluR protein abundance, localization, assembly, or receptor binding in human postmortem brain tissue. Of 532 records identified, 57 reports met eligibility criteria. Findings were synthesized narratively because of substantial heterogeneity in diagnoses, brain regions, receptor subtypes, and assays. Postmortem evidence was concentrated on mGluR5, mGluR2/3, and mGluR1, and on the prefrontal cortex, anterior cingulate cortex, and hippocampus. mGluR-related alterations were reported across disorders, including schizophrenia, major depressive disorder, Alzheimer disease, autism spectrum disorder, and alcohol use disorder. Although most analyses yielded null findings, the direction and magnitude of mGluR alterations varied across brain regions, receptor subtypes, and molecular endpoints. This inconsistency may partly reflect the distinct biological levels captured by transcript abundance, total protein, receptor assembly, localization, and ligand binding, together with regional, cell-type, disease-stage, and clinical heterogeneity. The available evidence therefore suggests context-dependent alterations in mGluR biology but not a uniform or disorder-specific molecular signature. Integration of postmortem findings with other approaches, including in vivo imaging, may clarify their biological and clinical significance.

neuroscience↗

A Novel Slow-Progressive Knee Osteoarthritis Murine Model Induced by Non-Invasive Posterior Cruciate Ligament Rupture in Mice

ObjectiveRecently, alternatives to animal testing, such as new approach methodologies, are being developed in the orthopedic research field; animal models still provide valuable insights into the pathogenesis of knee osteoarthritis (OA). However, commonly used models develop OA much more rapidly and severely than those observed in human patients. We aimed to develop a novel murine model that closely mimics the slow progression of human OA with posterior Cruciate ligament (PCL) rupture. Design12-week-old C57BL/6 mice were induced to PCL-rupture (PCL-R) by manually applying an external tibial posterior translation force. We analyzed joint kinematics, histological observations, and bone structure to confirm the absence of concurrent injury on day 0. Then, joint stability and the pathophysiological progression of knee OA were analyzed at 8, 16, and 34 weeks post-PCL-R. The destabilized medial meniscus (DMM) model was also analyzed to compare the OA progression. ResultsNon-invasive PCL-R intervention induced the complete rupture in the central region of PCL without concurrent injury. The PCL-R group showed larger posterior tibial deviation than the INTACT (P=0.008). Regarding the range of motion in the PCL-R group, there was no limitation in range of motion on day 0, but extension limitations occurred at weeks 16 and 34 weeks. Histologically, articular cartilage degeneration in PCL-R was milder than DMM. In the subchondral bone, micro-CT reconstruction images indicated that, compared with the INTACT group, the DMM group observed progressive subchondral bone formation from 16 weeks post-surgery. In contrast, the PCLR group maintained the subchondral bone structure even at 34 weeks. ConclusionsPCL-R model induced mild abnormal mechanical stress depending on posterior instability, and cartilage degeneration occurred more slowly in this model than in DMM models.

pathology↗

Dopamine shapes brain metastate dynamics

Dopamines influence on large-scale network dynamics, especially on the default mode network (DMN), remains uncertain, as fMRI studies have produced mixed results. One likely contributor to these discrepancies is reliance on traditional functional connectivity analyses, which typically derive a single metric (e.g., the Pearson correlation coefficient) from the entire time series and thus fail to capture network dynamics. To address this issue, we combined a dopaminergic challenge (mazindol, a dopamine transporter [DAT] reuptake inhibitor), PET, resting-state fMRI, and hidden Markov modeling (HMM) to characterize time-varying alterations in human large-scale functional networks following acute DAT blockade. We found that mazindol-induced increases in endogenous dopamine altered the balance between the brains functional "metastates," two recurrent higher-order network configurations that each encompass multiple HMM-derived brain states. Mazindol increased the time participants spent in an internally oriented cognitive metastate and decreased the time spent in a sensorimotor-perceptual metastate, with the DMN showing the most pronounced lengthening. In exploratory analyses, declines in [{superscript 1}{superscript 1}C]raclopride binding, a PET index of D2 dopamine receptor availability reflecting increased striatal extracellular dopamine levels, tended to show a positive correlation with the prolongation of these cognitive states. These findings indicate that dopamine is closely linked to shifts from sensorimotor and perceptual to cognitive brain metastates, potentially underpinning the prioritization of internally oriented over externally driven psychological processes. Our results highlight the importance of dynamic, time-resolved connectivity approaches for understanding neuromodulatory actions in the human brain and suggest that dopamine helps regulate the dynamic balance between functionally competing large-scale brain networks.

neuroscience↗

Novel Biomaterial-Based Synovial Fluid Analysis Reveals Protective microRNA Signatures in a Mouse Model of Acute Synovitis-Driven Osteoarthritis

Acute synovitis and continuous mechanical stress are critical factors of Post-traumatic Osteoarthritis (PTOA); however, the effect on cartilage degeneration and its underlying mechanisms remains unclear. Here, we established a novel biomaterial-based method for synovial fluid analysis in mice to uncover the mechanisms underlying the onset of PTOA, focusing on synovitis and mechanical stress. Twelve-week-old C57BL/6J males were divided to the ACL-Transection (ACL-T), ACL-rupture (ACL-R), and Intact groups. We performed joint instability test and histological analysis for cartilage degeneration and synovitis at 2, 6, and 10 weeks. Real time PCR was performed on articular cartilage at 2 weeks and synovium at 2, 6, and 10 weeks. Tetra-slime was injected into the knee joint, and solidified slime containing synovial fluid molecules was analyzed in digital PCR at 2 weeks. Acute synovitis and cartilage degeneration were induced in the ACL-T group at 2 weeks, although no difference was observed in joint instability between both two ACL injury models. Real time PCR showed significant increase of Mmp-3, Tnf-, Ifn-{gamma}, and inos in synovium of the ACL-T group. During this tissue interaction, although there were no significant differences, miR145-5p and miR149-5p in synovial fluid were also upregulated in the ACL-T group compared to the ACL-R group. Unlike the early stage, no histological or biological differences were observed between groups at 6 and 10 weeks. In conclusion, acute synovitis caused secondary cartilage degeneration via MMP-3 and TNF- in the synovium during the early stage and may involve M1 macrophage activation. Whereas it was suggested that synovial fluid miRNA might be produced to suppress the secondary cartilage degeneration. Furthermore, mechanical stress was the dominant factor in the late stage of OA, regardless of the initial synovitis condition.

pathology↗

Remote Cortical Network for Frontal Cognitive Symptoms derived from Tau Accumulation in Progressive Supranuclear Palsy

Progressive Supranuclear Palsy (PSP) is a neurodegenerative disorder characterized by impaired movement and frontal cognitive dysfunctions. While motor symptoms have been linked with subcortical tau deposits, network mechanisms underlying the frontal cognitive symptoms remain unclear because pathological tau accumulation is quite limited within the frontal cortex and heterogeneously distributed primarily in the subcortical regions. Here, we combined tau-PET using a high-contrast probe we have recently developed with normative connectome to resolve this issue. Tau-deposition sites were connected to a common cortical network that could not be identified through similar analyses based on atrophy detected by structural MRI. This network was predominantly overlapped with canonical action-mode and frontoparietal networks, which jointly support adaptive and goal-directed behavior. Critically, while the degree of subcortical primary tau deposition correlated with motor symptoms, only the degree of connectivity from tau-deposition sites to the derived cortical network explained the frontal cognitive deficits of individual patients. These findings suggest a novel mechanism that frontal cognitive impairments, but not motor deficits, in PSP are derived from remote effects of tau deposits, independent of atrophy, through the convergent connectivity to the identified common cortical network.

neuroscience↗

Effectiveness of Exercise Intervention in Preventing Active Arthritis Exacerbation in an SKG Mouse Model of Rheumatoid Arthritis

ObjectivesTo investigate the effects of low-intensity exercise on active arthritis in an SKG mouse model of human rheumatoid arthritis (RA) pathology. MethodsTwenty-four female SKG mice were divided into three groups: sedentary (control), AR (induced arthritis), and AREx (induced arthritis plus low-intensity exercise). Arthritis was induced via intraperitoneal administration of mannan. After a 2-week inflammation period, low-intensity treadmill exercise was performed only in the AREx group. Arthritis was assessed weekly during the rearing period. After 4 weeks of exercise, histological and bone morphometric analyses of the right ankle joint were performed. A histological analysis of the gastrocnemius muscle was also performed. Bulk mRNA sequencing was conducted on the left synovial membrane-fat pad (SM-FP) complex. ResultsThe synovitis score showed no change; however, the arthritis score was significantly lower in the AREx group than in the AR group (p<0.05), indicating that low-intensity exercise suppressed arthritis exacerbation. The calcaneal and talar bone volumes decreased in the AR group, whereas the AREx group showed no significant change. In the SM-FP complex tissue, the gene expression of inflammatory cytokines decreased in the AREx group compared with the AR group, particularly the suppression of IL6/Jak/Stat3. Immunohistochemical analysis revealed significantly decreased expression of pro-inflammatory cytokines and increased expression of anti-inflammatory cytokines in the synovium of the AREx group compared with the AR group (p<0.05). ConclusionLow-intensity exercise therapy for active RA showed anti-inflammatory and suppressive effects on arthritis exacerbation in SKG mice, a mouse model of human RA pathology. Key messagesO_LIExercise had an anti-inflammatory effect on SKG mice, a mouse model of rheumatoid arthritis. C_LIO_LIExercise suppresses pro-inflammatory cytokine pathways such as IL6/Jak/Stat3 signalling in the synovial-fat complex tissue. C_LIO_LIExercise therapy is effective in improving the pathophysiology of active rheumatoid arthritis. C_LI

molecular biology↗

Concurrent Joint Contact in Anterior Cruciate Ligament Injury induces cartilage micro-injury and subchondral bone sclerosis, resulting in knee osteoarthritis

ObjectiveAnterior Cruciate Ligament (ACL) injury initiates post-traumatic osteoarthritis (PTOA) via two distinct processes: initial direct contact injury of the cartilage surface during ACL injury, and secondary joint instability due to the ACL deficiency. Using the well-established Compression-induced ACL rupture method (ACL-R) and a novel Non-Compression ACL-R model, we aimed to reveal the individual effects of cartilage compression and joint instability on PTOA progression after ACL injury in mice. DesignTwelve-week-old C57BL/6J male were randomly divided to three experimental groups: Compression ACL-R, Non-Compression ACL-R, and Intact. Following ACL injury, we performed joint laxity testing and microscopic analysis of the articular cartilage surface at 0 days, in vivo optical imaging of matrix-metalloproteinase (MMP) activity at 3 and 7 days, and histological and microCT analysis at 0, 7, 14, and 28 days. ResultsThe Compression ACL-R group exhibited a significant increase of cartilage roughness immediately after injury compared with the Non-Compression group. At 7 days, the Compression group exhibited increased MMP-induced fluorescence intensity and MMP-13 positive cell ratio of chondrocytes. Moreover, histological cartilage degeneration was observable in the Compression group at the same time point. Sclerosis of tibial subchondral bone in the Compression group was more significantly developed than in the Non-Compression group at 28 days. ConclusionsBoth Compression and Non-Compression ACL injury initiated PTOA progression due to joint instability. However, joint contact during ACL rupture also caused initial micro-damage on the cartilage surface and initiated early MMP activity, which could accelerate PTOA progression compared to ACL injury without concurrent joint contact.

molecular biology↗

Muscle Contraction is Essential for Tendon Healing and Muscle Function Recovery after Achilles Tendon Rupture and Surgical Repair

Incomplete tendon healing and postponed muscle weakness after Achilles tendon rupture and surgical repair lead to poor performance in patient activities. Although the effectiveness of postoperative early functional rehabilitation has been proven, the priority and each effect of specific methods in early rehabilitation remain unclear. We hypothesized early muscle contraction exercises without joint motion would promote tendon healing and prevent calf muscle atrophy; in contrast, early static stretching after surgical repair would not contribute to tendon healing and induce calf muscle atrophy. C57Bl/6 mice underwent Achilles tendon rupture and suture repair, followed by different methods of post-surgery interventions: a non-exercise group, a Static stretching group, and an Electrical muscle stimulation group. 3 and 5 weeks after surgery, we assessed ex vivo tendon mechanical properties, collagen fiber alignment, and histological muscle properties. Electrical Muscle Stimulation restored the recovery of tendon mechanical properties and muscle strength more quickly than Static stretching. Static stretching had no additional effect on them compared to the non-exercise. Our results suggested that calf muscle contraction was essential as a post-surgery early functional rehabilitation to load tensile forces on tendons and improve Achilles tendon healing. Additionally, early muscle contractions naturally promote restoring muscle function after the rupture, but further research is needed to optimize muscle contraction protocols. Statement of Clinical SignificanceThis study shows the importance of selecting appropriate exercise modalities to resolve imperfections in tendon healing and muscle recovery. The establishment of proper rehabilitation is expected to improve post-surgery outcomes. Study DesignA controlled laboratory study.

physiology↗

Characteristic differences in tibial subchondral bone changes in the post-traumatic knee osteoarthritis model

ObjectiveMeniscus degeneration and subchondral bone changes contribute to the development and progression of knee OA. The purpose of this study was to reveal the relationship between medial meniscus degeneration and characteristics of subchondral bone changes in different models DesignWe used the anterior cruciate ligament transection (ACL-T) model, destabilization of the medial meniscus (DMM) model, controlled abnormal tibial translation (CATT) model and a controlled abnormal tibial rotation (CATR) model with different mechanical stresses. We performed histological analysis and micro computed tomography analysis, at 4 and 6 weeks. In addition, we divided the tibial subchondral bone into four compartments and set the regions of interest ResultsMeniscus degeneration was observed in all groups, but there was no significant difference. The ACL-T group showed posterior displacement of the contact area, and the DMM and CATR groups showed lateral deviation of the medial meniscus. The region-specific subchondral bone changes in each model showed that changes in mechanical stress due to ACL and meniscus dysfunction, as well as changes in the contact area, affect the bony structure of the subchondral bone differently in each region. ConclusionsSubchondral bone changes in different models of mechanical stress were different in each region. In particular, changes in the contact area and increased compressive stress due to meniscus dysfunction were suggested to promote bone formation. The results of this study indicate that changes in alignment and contact area in the PTOA model may cause region-specific characteristics of the subchondral bone changes.

pathology↗

Abnormal Tibia Translation leads Directly the Surface Cartilage Degeneration with Molecular Biological Response using a Novel Non-Invasive ACL ruptured Mice Model

ObjectiveThe ACL-deficient model helps to clarify the mechanism of knee OA; however, the conventional ACL injury model could have included concurrent onset factors such as direct compression stress to cartilage and subchondral bone. In this study, we established a novel Non-invasive ACL-Ruptured mouse model without concurrent injuries and elucidated the relationship between OA progression and joint instability. DesignWe induced the ACL-Rupture non-invasively in twelve-week-old C57BL/6 male mice and evaluated histological, macroscopical, and morphological analysis at 0 days. Next, we created the ACL-R, controlled abnormal tibial translation (CATT), and Sham groups. Then, the joint stability and OA pathophysiology were analyzed at 2, 4, and 8 weeks. ResultsNo intra-articular injuries, except for ACL rupture, were observed in the ACL-R model. ACL-R mice increased anterior tibial displacement compared to the Sham group (p<0.001, 95% CI [-1.509 to -0.966]) and CATT group (p<0.001, 95% CI [-0.841 to -0.298]) at 8 weeks. All mice in the ACL-R group caused cartilage degeneration. The degree of cartilage degeneration in the ACL-R group was higher than in the CATT group (p=0.006) at 8 weeks. The MMP-3-positive cell rate of chondrocytes increased in the ACL-R group than CATT group from 4 weeks (p=0.043; 95% CI [-28.32 to -0.364]) while that of synovial cells increased at 8 weeks (p=0.031; 95% CI [-23.398 to -1.021]). ConclusionWe successfully established a Non-invasive ACL-R model without intra-articular damage. Our model revealed that chondrocytes might react to abnormal mechanical stress prior to synovial cells while the knee OA onset.

molecular biology↗

Serotonergic neural network related to behavioral inhibition system

Rationale The tendency to avoid punishment, called behavioral inhibition system, is an essential aspect of motivational behavior. Behavioral inhibition system is related to negative affect, such as anxiety, depression and pain, but its neural basis has not yet been clarified. Objectives To clarify the association between individual variations in behavioral inhibition system and brain 5-HT2A receptor availability and specify which brain networks were involved in healthy male subjects, using [18F]altanserin positron emission tomography and resting-state functional magnetic resonance imaging. Results Behavioral inhibition system score negatively correlated with 5-HT2A receptor availability in anterior cingulate cortex. A statistical model indicated that the behavioral inhibition system score was associated with 5-HT2A receptor availability, which was mediated by the functional connectivity between anterior cingulate cortex and left middle frontal gyrus, both of which involved in the cognitive control of negative information processing. Conclusions Individuals with high behavioral inhibition system displays low 5-HT2A receptor availability in anterior cingulate cortex and this cognitive control network links with prefrontal-cingulate integrity. These findings have implications for underlying the serotonergic basis of physiologies in aversion.

neuroscience↗

Effect of differences in mechanical stress in vivo on the onset and progression of knee osteoarthritis

ObjectiveThe effect of the type of mechanical stress on OA onset has not been clarified. The aim of this study was to establish a new model that reproduces the type and increase and decrease of mechanical stress in vivo and to clarify the differences in the mechanism of knee OA onset and progression among the models. DesignTo reproduce the difference in mechanical stress, we used the anterior cruciate ligament transection (ACL-T) model and the destabilization of the medial meniscus (DMM) model. In addition, we created a controlled abnormal tibial translation (CATT) model and a controlled abnormal tibial rotation (CATR) model that suppressed the joint instability of the ACL-T and DMM model, respectively. These four models reproduced the increase and decrease in shear force due to joint instability and compressive stress due to meniscal dysfunction. We performed joint instability analysis with soft X-ray, micro computed tomography analysis, histological analysis, and immunohistological analysis in 4 and 6 weeks. ResultsJoint instability decreased in the CATT and CATR groups. The meniscus deviated in the DMM and CATR groups. Chondrocyte hypertrophy increased in the ACL-T and DMM groups with joint instability. In the subchondral bone, bone resorption was promoted in the ACL-T and CATT groups, and bone formation was promoted in the DMM and CATR groups. ConclusionsIncreased shear force causes articular cartilage degeneration and osteoclast activation in the subchondral bone. In contrast, increased compressive stress promotes bone formation in the subchondral bone earlier than articular cartilage degeneration occurs.

pathology↗

Effect of Suppression of Rotational Joint Instability on Cartilage and Meniscus Degeneration in Mouse Osteoarthritis Model

ObjectiveJoint instability and meniscal dysfunction contribute to the onset and progression of knee osteoarthritis (OA). In the destabilization of the medial meniscus (DMM) model, secondary OA occurs due to the rotational instability and increases compressive stress resulting from the meniscal dysfunction. We created a new controlled abnormal tibial rotation (CATR) model that reduces the rotational instability that occurs in the DMM model. So, we aimed to investigate whether rotational instability affects articular cartilage degeneration using the DMM and CATR models, as confirmed using histology and immunohistochemistry. DesignTwelve-week-old male mice were randomized into 3 groups: DMM group, CATR group, and INTACT group (right knee of the DMM group). After 8 and 12 weeks, we performed the tibial rotational test, safranin-O/fast green staining, and immunohistochemical staining for TNF- and MMP-13. ResultsThe rotational instability in the DMM group was significantly higher than that of the other groups. And articular cartilage degeneration was higher in the DMM group than in the other groups. However, meniscal degeneration was observed in both DMM and CATR groups. The TNF- and MMP-13 positive cell rates in the articular cartilage of the CATR group were lower than those in the DMM group. ConclusionsWe found that the articular cartilage degeneration was effectively suppressed by controlling the rotational instability caused by meniscal dysfunction. These findings suggest that suppression of rotational instability in the knee joint is an effective therapeutic measure for preventing OA progression.

pathology↗