Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Osthole, an effective monomer in Chinese medicinal herbs, can cross the blood-brain barrier and protect against brain injury, with few toxic effects. In this study, a rat model of Alzheimer's disease was established after intracerebroventricular injection of β-amyloid peptide (25-35). Subsequently, the rats were intraperitoneally treated with osthole (12.5 or 25.0 mg/kg) for 14 successive days. Results showed that osthole treatment significantly improved cognitive impairment and protected hippocampal neurons of Alzheimer's disease rats. Also, osthole treatment alleviated suppressed long-term potentiation in the hippocampus of Alzheimer's disease rats. In these osthole-treated Alzheimer's disease rats, the level of glutamate decreased, but there was no significant change in γ-amino-butyric acid. These experimental findings suggest that osthole can improve learning and memory impairment, and increase synaptic plasticity in Alzheimer's disease rats. These effects of osthole may be because of its regulation of central glutamate and γ-amino-butyric acid levels.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4268736 | PMC |
| http://dx.doi.org/10.3969/j.issn.1673-5374.2012.30.001 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Estimated Glucose Disposal Rate and Risk of Stroke and Dementia in Nondiabetics: A UK Biobank Prospective Cohort Study.
Arterioscler Thromb Vasc Biol
September 2025
Institute of Cardiovascular Diseases and Department of Cardiology, Ultrasound in Cardiac Electrophysiology and Biomechanics Key Laboratory of Sichuan Province, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu (K.L., H.M., W.J
Background: The estimated glucose disposal rate (eGDR) is a validated surrogate marker of insulin resistance. However, its association with stroke and dementia in nondiabetic populations remains insufficiently investigated.
Methods: This prospective cohort study included nondiabetic participants from the UK Biobank.
Concussive injuries induce neuronal stress-dependent tau mislocalization to dendritic spines with acrolein and functional network alteration in TBI-on-a-chip.
Lab Chip
September 2025
Weldon School of Biomedical Engineering, Purdue University, West Lafayette, IN 47907, USA.
Traumatic brain injuries (TBIs) are a risk factor for Alzheimer's disease (AD), and share several important pathological features including the development of neurofibrillary tangles (NFT) of tau protein. While this association is well established, the underlying pathogenesis is poorly defined and current treatment options remain limited, necessitating novel methods and approaches. In response we developed "TBI-on-a-chip", an trauma model utilizing murine cortical networks on microelectrode arrays (MEAs), capable of reproducing clinically relevant impact injuries while providing simultaneous morphological and electrophysiological readout.
View Article and Find Full Text PDF14-3-3 Proteins Negatively Regulate Microglial Activation via Inhibition of the NF-κB Pathway.
J Neurochem
September 2025
Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Microglia, the resident immune cells of the central nervous system (CNS), are involved in the pathogenesis of neurodegenerative diseases, such as Alzheimer's disease (AD), Dementia with Lewy Bodies (DLB), and Parkinson's disease (PD). 14-3-3 proteins act as molecular hubs to regulate protein-protein interactions, which are involved in numerous cellular functions, including cellular signaling, protein folding, and apoptosis. We previously revealed decreased 14-3-3 levels in the brains of human subjects with neurodegenerative diseases.
View Article and Find Full Text PDFCase Study 10: A 51-Year-Old Man With Psychosis, Decline in Self-Care, and Cognitive Deterioration.
J Neuropsychiatry Clin Neurosci
September 2025
Departments of Psychiatry and Neurology, Center for Brain/Mind Medicine, and Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston.
Neuroinflammation has emerged as a central and dynamic component of the pathophysiology underlying a wide range of neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease, and multiple sclerosis. Far from being a secondary consequence of neuronal damage, inflammatory processes (mediated by microglia, astrocytes, peripheral immune cells, and associated molecular mediators) actively shape disease onset, progression, and symptomatology. This review synthesizes current knowledge on the cellular and molecular mechanisms that govern neuroinflammatory responses, emphasizing both shared and disease-specific pathways.
View Article and Find Full Text PDF