Brain and Nerve最新文献_第3页

[Mechanisms of High-Level Human Visual Cognition and Associated Disorders]. [高级人类视觉认知和相关疾病的机制]。

Brain and Nerve Pub Date : 2026-08-01 DOI: 10.11477/mf.188160960780080923

Kyoko Suzuki

{"title":"[Mechanisms of High-Level Human Visual Cognition and Associated Disorders].","authors":"Kyoko Suzuki","doi":"10.11477/mf.188160960780080923","DOIUrl":"https://doi.org/10.11477/mf.188160960780080923","url":null,"abstract":"Human visual cognition relies on two major streams that originate in the primary visual cortex: the ventral stream, which projects to the temporal lobe, and the dorsal stream, which projects to the parietal lobe. The ventral stream processes visual features such as shape, color, and texture, which are integrated to support object recognition. Within this stream, cortical regions are further organized by stimulus categories, including faces, places, words, and objects. The dorsal stream links vision with action and spatial behavior and can be subdivided into two functional substreams. The dorso-dorsal stream, centered on the superior parietal lobule, mediates online visuomotor control and reaching movements. The ventro-dorsal stream, associated with the inferior parietal lobule, contributes to object-related actions and spatial cognition. Damage to these streams produces dissociable clinical syndromes, such as visual agnosia following ventral stream damage and visual inattention after dorsal stream damage. While previous studies have mainly examined visual cognitive dysfunction due to focal lesions, neurodegenerative disorders also provide a unique opportunity to investigate visual network vulnerability. Conditions such as posterior cortical atrophy and dementia with Lewy bodies exhibit characteristic visuocognitive impairments that reflect systematic neuronal degeneration. Analyzing symptom profiles in such disorders may clarify the functional segregation of the visual streams.","PeriodicalId":52507,"journal":{"name":"Brain and Nerve","volume":"78 8","pages":"923-930"},"PeriodicalIF":0.0,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148801261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

[Immune Checkpoint Tim-3 Regulates Microglial Function in Alzheimer's Disease]. 免疫检查点Tim-3调节阿尔茨海默病的小胶质细胞功能。

Brain and Nerve Pub Date : 2026-08-01 DOI: 10.11477/mf.188160960780080931

Kimitoshi Kimura

{"title":"[Immune Checkpoint Tim-3 Regulates Microglial Function in Alzheimer's Disease].","authors":"Kimitoshi Kimura","doi":"10.11477/mf.188160960780080931","DOIUrl":"10.11477/mf.188160960780080931","url":null,"abstract":"Microglia are resident immune cells of the central nervous system and play a central role in the pathogenesis of Alzheimer's disease (AD). Emerging evidence indicates that their functional state critically influences amyloid-β (Aβ) clearance, neuroinflammation, and disease progression. Tim-3, an immune checkpoint molecule, is highly expressed in microglia and functions as a key regulator of microglial homeostasis through the transforming growth factor-β (TGF-β)-Smad2 signaling pathway. Microglia-specific deletion of Tim-3 enhances phagocytic activity. Moreover, microglia-specific Tim-3 deficiency results in reduced Aβ deposition, decreased neurotoxicity, and improved cognitive performance in the 5xFAD mouse model of AD. These effects are not mediated by changes in Aβ production but rather by enhanced microglial clearance and remodeling of Aβ plaques into less toxic forms. Furthermore, single-cell analyses reveal that Tim-3 deficiency promotes a microglial state characterized by increased phagocytic capacity and reduced pro-inflammatory signaling. These findings suggest that Tim-3 acts as a functional checkpoint that limits beneficial microglial responses in AD and that targeting Tim-3 may therefore represent a promising therapeutic strategy for reprogramming microglia and improving disease outcomes.","PeriodicalId":52507,"journal":{"name":"Brain and Nerve","volume":"78 8","pages":"931-937"},"PeriodicalIF":0.0,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148801311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

[Peripheral Autonomic Neuropathy in α-Synucleinopathy]. [α-突触核蛋白病的周围自主神经病变]。

Brain and Nerve Pub Date : 2026-08-01 DOI: 10.11477/mf.188160960780080889

Kaoru Yagita, Masaki Takao

引用次数: 0

[Diabetic Autonomic Neuropathy]. [糖尿病自主神经病变]。

Brain and Nerve Pub Date : 2026-08-01 DOI: 10.11477/mf.188160960780080893

Sonoko Misawa

{"title":"[Diabetic Autonomic Neuropathy].","authors":"Sonoko Misawa","doi":"10.11477/mf.188160960780080893","DOIUrl":"10.11477/mf.188160960780080893","url":null,"abstract":"Diabetic autonomic neuropathy is a clinically important component of diabetic neuropathy involving the cardiovascular, gastrointestinal, genitourinary, sudomotor, pupillary, and glucose counterregulatory systems. Cardiovascular autonomic neuropathy (CAN) has been extensively studied and is clinically relevant because of its association with adverse cardiovascular and renal outcomes. Early CAN is frequently silent and may only be recognized by reduced heart rate variability or abnormal cardiovascular autonomic reflex testing. As CAN progresses, patients develop resting tachycardia, reduced exercise tolerance, orthostatic or postprandial hypotension, abnormal nocturnal blood pressure regulation, and perioperative hemodynamic instability. Non-cardiovascular manifestations include gastroparesis, bowel and bladder dysfunction, erectile dysfunction, sudomotor and pupillary abnormalities, and impaired hypoglycemic awareness. The underlying mechanisms involve chronic hyperglycemia, glycemic variability, dyslipidemia, insulin resistance, oxidative and mitochondrial stress, inflammation, microvascular injury, and impaired axon-glial support. Clinically, evaluation should begin with a systematic symptom review, neurological examination, supine and standing blood pressure measurements, and heart rate assessment, followed by organ-specific testing if indicated. Treatment was based on comprehensive risk factor control and symptom-directed management.","PeriodicalId":52507,"journal":{"name":"Brain and Nerve","volume":"78 8","pages":"893-897"},"PeriodicalIF":0.0,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148801327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

[Autoimmune Autonomic Ganglionopathy]. 自身免疫性自主神经节病

Brain and Nerve Pub Date : 2026-08-01 DOI: 10.11477/mf.188160960780080905

Shunya Nakane

引用次数: 0

[Autonomic Dysfunction in ATTR Amyloidosis]. ATTR淀粉样变性的自主神经功能障碍。

Brain and Nerve Pub Date : 2026-08-01 DOI: 10.11477/mf.188160960780080899

Minori Kodaira, Yoshiki Sekijima

引用次数: 0

[Control of Social Behavior by Prefrontal-Paraventricular Thalamic Circuits Shaped by Developmental Social Experience]. 发展性社会经验塑造的前额叶-室旁丘脑回路对社会行为的控制。

Brain and Nerve Pub Date : 2026-07-01 DOI: 10.11477/mf.188160960780070781

Kazuhiko Yamamuro