pubmed_fetch_contents_example.mdā¢14.5 kB
Tool Call Arguments:
```json
{
"pmids": ["39715098", "39359093", "39704040"],
"detailLevel": "abstract_plus",
"includeMeshTerms": true,
"includeGrantInfo": true,
"outputFormat": "json"
}
```
Tool Response:
```json
{
"requestedPmids": ["39715098", "39359093", "39704040"],
"articles": [
{
"pmid": "39715098",
"title": "The compound (E)-2-(3,4-dihydroxystyryl)-3-hydroxy-4H-pyran-4-one alleviates neuroinflammation and cognitive impairment in a mouse model of Alzheimer's disease.",
"abstractText": "JOURNAL/nrgr/04.03/01300535-202511000-00034/figure1/v/2024-12-20T164640Z/r/image-tiff Previous studies have shown that the compound (E)-2-(3,4-dihydroxystyryl)-3-hydroxy-4H-pyran-4-one (D30), a pyromeconic acid derivative, possesses antioxidant and anti-inflammatory properties, inhibits amyloid-β aggregation, and alleviates scopolamine-induced cognitive impairment, similar to the phase III clinical drug resveratrol. In this study, we established a mouse model of Alzheimer's disease via intracerebroventricular injection of fibrillar amyloid-β to investigate the effect of D30 on fibrillar amyloid-β-induced neuropathology. Our results showed that D30 alleviated fibrillar amyloid-β-induced cognitive impairment, promoted fibrillar amyloid-β clearance from the hippocampus and cortex, suppressed oxidative stress, and inhibited activation of microglia and astrocytes. D30 also reversed the fibrillar amyloid-β-induced loss of dendritic spines and synaptic protein expression. Notably, we demonstrated that exogenous fibrillar amyloid-β introduced by intracerebroventricular injection greatly increased galectin-3 expression levels in the brain, and this increase was blocked by D30. Considering the role of D30 in clearing amyloid-β, inhibiting neuroinflammation, protecting synapses, and improving cognition, this study highlights the potential of galectin-3 as a promising treatment target for patients with Alzheimer's disease.",
"authors": [
{
"lastName": "Liu",
"firstName": "Xueyan",
"initials": "X",
"affiliation": "Department of Medicinal Chemistry, School of Pharmacy, Fujian Medical University, Fuzhou, Fujian Province, China."
},
{
"lastName": "Wu",
"firstName": "Wei",
"initials": "W",
"affiliation": "Fujian Provincial Key Laboratory of Brain Aging and Neurodegenerative Diseases, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, Fujian Province, China."
},
{
"lastName": "Li",
"firstName": "Xuejuan",
"initials": "X",
"affiliation": "Department of Medicinal Chemistry, School of Pharmacy, Fujian Medical University, Fuzhou, Fujian Province, China."
},
{
"lastName": "Wang",
"firstName": "Chengyan",
"initials": "C",
"affiliation": "Institute of Laboratory Animal Center, Fujian Medical University, Fuzhou, Fujian Province, China."
},
{
"lastName": "Chai",
"firstName": "Ke",
"initials": "K",
"affiliation": "Fujian Provincial Key Laboratory of Brain Aging and Neurodegenerative Diseases, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, Fujian Province, China."
},
{
"lastName": "Yuan",
"firstName": "Fanru",
"initials": "F",
"affiliation": "Department of Medicinal Chemistry, School of Pharmacy, Fujian Medical University, Fuzhou, Fujian Province, China."
},
{
"lastName": "Zheng",
"firstName": "Huijuan",
"initials": "H",
"affiliation": "Department of Medicinal Chemistry, School of Pharmacy, Fujian Medical University, Fuzhou, Fujian Province, China."
},
{
"lastName": "Yao",
"firstName": "Yuxing",
"initials": "Y",
"affiliation": "Department of Medicinal Chemistry, School of Pharmacy, Fujian Medical University, Fuzhou, Fujian Province, China."
},
{
"lastName": "Li",
"firstName": "Chenlu",
"initials": "C",
"affiliation": "Department of Neurosurgery, Neurosurgery Research Institute, The First Affiliated Hospital, Fujian Medical University, Fuzhou, Fujian Province, China."
},
{
"lastName": "Ye",
"firstName": "Zu-Cheng",
"initials": "ZC",
"affiliation": "Fujian Provincial Key Laboratory of Brain Aging and Neurodegenerative Diseases, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, Fujian Province, China."
},
{
"lastName": "Zha",
"firstName": "Daijun",
"initials": "D",
"affiliation": "Department of Medicinal Chemistry, School of Pharmacy, Fujian Medical University, Fuzhou, Fujian Province, China."
}
],
"journalInfo": {
"title": "Neural regeneration research",
"isoAbbreviation": "Neural Regen Res",
"volume": "20",
"issue": "11",
"pages": "3330-3344",
"publicationDate": { "year": "2025", "month": "Nov", "day": "1" }
},
"publicationTypes": ["Journal Article"],
"doi": "10.4103/NRR.NRR-D-23-01890",
"articleDates": [
{ "dateType": "Electronic", "year": "2024", "month": "7", "day": "10" }
]
},
{
"pmid": "39359093",
"title": "The cGAS-STING-interferon regulatory factor 7 pathway regulates neuroinflammation in Parkinson's disease.",
"abstractText": "JOURNAL/nrgr/04.03/01300535-202508000-00026/figure1/v/2024-09-30T120553Z/r/image-tiff Interferon regulatory factor 7 plays a crucial role in the innate immune response. However, whether interferon regulatory factor 7-mediated signaling contributes to Parkinson's disease remains unknown. Here we report that interferon regulatory factor 7 is markedly up-regulated in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced mouse model of Parkinson's disease and co-localizes with microglial cells. Both the selective cyclic guanosine monophosphate adenosine monophosphate synthase inhibitor RU.521 and the stimulator of interferon genes inhibitor H151 effectively suppressed interferon regulatory factor 7 activation in BV2 microglia exposed to 1-methyl-4-phenylpyridinium and inhibited transformation of mouse BV2 microglia into the neurotoxic M1 phenotype. In addition, siRNA-mediated knockdown of interferon regulatory factor 7 expression in BV2 microglia reduced the expression of inducible nitric oxide synthase, tumor necrosis factor α, CD16, CD32, and CD86 and increased the expression of the anti-inflammatory markers ARG1 and YM1. Taken together, our findings indicate that the cyclic guanosine monophosphate adenosine monophosphate synthase-stimulator of interferon genes-interferon regulatory factor 7 pathway plays a crucial role in the pathogenesis of Parkinson's disease.",
"authors": [
{
"lastName": "Zhou",
"firstName": "Shengyang",
"initials": "S",
"affiliation": "Laboratory of Neurodegenerative and Neuroinjury Diseases, Wuxi Medicine School, Jiangnan University, Wuxi, Jiangsu Province, China."
},
{ "lastName": "Li", "firstName": "Ting", "initials": "T" },
{ "lastName": "Zhang", "firstName": "Wei", "initials": "W" },
{ "lastName": "Wu", "firstName": "Jian", "initials": "J" },
{ "lastName": "Hong", "firstName": "Hui", "initials": "H" },
{ "lastName": "Quan", "firstName": "Wei", "initials": "W" },
{ "lastName": "Qiao", "firstName": "Xinyu", "initials": "X" },
{ "lastName": "Cui", "firstName": "Chun", "initials": "C" },
{ "lastName": "Qiao", "firstName": "Chenmeng", "initials": "C" },
{ "lastName": "Zhao", "firstName": "Weijiang", "initials": "W" },
{ "lastName": "Shen", "firstName": "Yanqin", "initials": "Y" }
],
"journalInfo": {
"title": "Neural regeneration research",
"isoAbbreviation": "Neural Regen Res",
"volume": "20",
"issue": "8",
"pages": "2361-2372",
"publicationDate": { "year": "2025", "month": "Aug", "day": "1" }
},
"publicationTypes": ["Journal Article"],
"doi": "10.4103/NRR.NRR-D-23-01684",
"articleDates": [
{ "dateType": "Electronic", "year": "2024", "month": "6", "day": "3" }
]
},
{
"pmid": "39704040",
"title": "α-Synuclein in Parkinson's Disease: From Bench to Bedside.",
"abstractText": "α-Synuclein (α-syn), a pathological hallmark of PD, is emerging as a bridging element at the crossroads between neuro/immune-inflammatory responses and neurodegeneration in PD. Several evidence show that pathological α-syn accumulates in neuronal and non-neuronal cells (i.e., neurons, microglia, macrophages, skin cells, and intestinal cells) in central and peripheral tissues since the prodromal phase of the disease, contributing to brain pathology. Indeed, pathological α-syn deposition can promote neurogenic/immune-inflammatory responses that contribute to systemic and central neuroinflammation associated with PD. After providing an overview of the structure and functions of physiological α-syn as well as its pathological forms, we review current studies about the role of neuronal and non-neuronal α-syn at the crossroads between neuroinflammation and neurodegeneration in PD. In addition, we provide an overview of the correlation between the accumulation of α-syn in central and peripheral tissues and PD, related symptoms, and neuroinflammation. Special attention was paid to discussing whether targeting α-syn can represent a suitable therapeutical approach for PD.",
"authors": [
{
"lastName": "Bellini",
"firstName": "Gabriele",
"initials": "G",
"affiliation": "Center for Neurodegenerative Diseases, Unit of Neurology, Parkinson's Disease and Movement Disorders, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy."
},
{
"lastName": "D'Antongiovanni",
"firstName": "Vanessa",
"initials": "V",
"affiliation": "Unit of Histology and Embryology, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy."
},
{
"lastName": "Palermo",
"firstName": "Giovanni",
"initials": "G",
"affiliation": "Center for Neurodegenerative Diseases, Unit of Neurology, Parkinson's Disease and Movement Disorders, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy."
},
{
"lastName": "Antonioli",
"firstName": "Luca",
"initials": "L",
"affiliation": "Unit of Pharmacology and Pharmacovigilance, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy."
},
{
"lastName": "Fornai",
"firstName": "Matteo",
"initials": "M",
"affiliation": "Unit of Pharmacology and Pharmacovigilance, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy."
},
{
"lastName": "Ceravolo",
"firstName": "Roberto",
"initials": "R",
"affiliation": "Center for Neurodegenerative Diseases, Unit of Neurology, Parkinson's Disease and Movement Disorders, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy."
},
{
"lastName": "Bernardini",
"firstName": "Nunzia",
"initials": "N",
"affiliation": "Unit of Histology and Embryology, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy."
},
{
"lastName": "Derkinderen",
"firstName": "Pascal",
"initials": "P",
"affiliation": "Department of Neurology, Nantes Université, CHU Nantes, INSERM, Nantes, France."
},
{
"lastName": "Pellegrini",
"firstName": "Carolina",
"initials": "C",
"affiliation": "Unit of Histology and Embryology, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy."
}
],
"journalInfo": {
"title": "Medicinal research reviews",
"isoAbbreviation": "Med Res Rev",
"volume": "45",
"issue": "3",
"pages": "909-946",
"publicationDate": { "year": "2025", "month": "May" }
},
"publicationTypes": ["Journal Article", "Review"],
"doi": "10.1002/med.22091",
"articleDates": [
{ "dateType": "Electronic", "year": "2024", "month": "12", "day": "20" }
],
"meshTerms": [
{
"descriptorName": "Humans",
"descriptorUi": "D006801",
"isMajorTopic": false
},
{
"descriptorName": "alpha-Synuclein",
"descriptorUi": "D051844",
"qualifierName": "metabolism",
"qualifierUi": "Q000378",
"isMajorTopic": true
},
{
"descriptorName": "Parkinson Disease",
"descriptorUi": "D010300",
"qualifierName": "metabolism",
"qualifierUi": "Q000378",
"isMajorTopic": true
},
{
"descriptorName": "Animals",
"descriptorUi": "D000818",
"isMajorTopic": false
},
{
"descriptorName": "Translational Research, Biomedical",
"descriptorUi": "D057170",
"isMajorTopic": true
},
{
"descriptorName": "Inflammation",
"descriptorUi": "D007249",
"isMajorTopic": false
},
{
"descriptorName": "Neurons",
"descriptorUi": "D009474",
"qualifierName": "metabolism",
"qualifierUi": "Q000378",
"isMajorTopic": false
}
],
"grantList": [
{ "agency": "The authors received no specific funding for this work." }
]
}
],
"notFoundPmids": [],
"eFetchDetails": {
"urls": [
"https://eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=pubmed&id=39715098%2C39359093%2C39704040&retmode=xml"
],
"requestMethod": "GET"
}
}
```