The aim of this study was to investigate the correlation between brain-derived neurotrophic factor (BDNF) expression and cognitive impairment in post‑stroke depression (PSD) rats and to explore the mechanism(s) involved in the process of cognitive impairment. A rat model of focal cerebral ischemia was established by occluding the middle cerebral artery (MCA). Rats were subjected to isolation-housing combined with chronic unexpected mild stress (CUMS) to establish a PSD rat model. The learning and memory abilities of the PSD rat model were evaluated by passive avoidance tests. Real‑time PCR and immunohistochemical methods were used to detect changes in BDNF mRNA and protein expression in the hippocampus. Passive avoidance defects were revealed in the PSD and depression groups. Passive avoidance defects were more evident in the PSD group compared with the depression group and the difference was statistically significant (P<0.05). BDNF expression in the hippocampus was significantly lower in the PSD and depression groups compared with that in the normal control group (P<0.01). No significant difference in BDNF expression was identified between the normal control and stroke groups (P>0.05) or between the PSD and the depression groups (P>0.05). The decrease in BDNF expression in the hippocampus of PSD rats may aggravate cognitive impairment, however, the degree of cognitive impairment cannot be reflected by the expression levels of BDNF in the hippocampus.
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http://dx.doi.org/10.3892/mmr.2012.1009 | DOI Listing |
J Neuroinflammation
December 2024
Research Institute for Medicines (iMed.ULisboa), Faculdade de Farmácia, Universidade de Lisboa, Lisboa, Portugal.
Multiple Sclerosis (MS), a neuroinflammatory disease of the central nervous system, is one of the commonest causes of non-traumatic disability among young adults. Impaired cognition arises as an impactful symptom affecting more than 50% of the patients and with substantial impact on social, economic, and individual wellbeing. Despite the lack of therapeutic strategies, many efforts have been made to understand the mechanisms behind cognitive impairment in MS patients.
View Article and Find Full Text PDFBMC Public Health
December 2024
Experimental Research Unit, Faculty of Medicine, National Autonomous University of Mexico, Dr. Balmis 148. Col. Doctores, Alcaldía Cuauhtémoc. CP 06720, Mexico City, Mexico.
Background: There is limited population-based evidence on the prevalence of cognitive impairment in Mexico, a country with a rapidly aging population and where key risk factors, such as diabetes and obesity, are common. This study describes the distribution of cognitive impairment in adults from Mexico City.
Methods: This cross-sectional population-based study included participants from the Mexico City Prospective Study which recruited 150,000 adults aged ≥ 35 years in 1998-2004.
BMC Psychiatry
December 2024
Department of Geriatric Psychiatry, Suzhou Mental Health Center, Suzhou Guangji Hospital, the Affiliated Guangji Hospital of Soochow University, Suzhou, China.
Background: Cognitive impairment is prevalent in bipolar disorder (BD), and has negative impacts on functional impairments and quality of life, despite euthymic states in most individuals. The underlying neurobiological basis of cognitive impairment in BD is still unclear.
Methods: To further explore potential connectivity abnormalities and their associations with cognitive impairment, we conducted a degree centrality (DC) analysis and DC (seed)-based functional connectivity (FC) approach in unmedicated, euthymic individuals with BD.
Cell Mol Immunol
January 2025
Department of Geriatrics, Gerontology Institute of Anhui Province, The First Affiliated Hospital of University of Science and Technology of China, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230001, China.
Microglia dysfunction-associated neuroinflammation is an important driver of Alzheimer's disease (AD), but the mechanism is poorly understood. Here, we show that demyelination promotes neuroinflammation and cognitive impairment via the lysophosphatidylserine (LysoPS)-GPR34 axis in AD. Demyelination is observed at the early stage and is accompanied by an increase in LysoPS in myelin debris in a 5xFAD mouse model of AD.
View Article and Find Full Text PDFSci Rep
December 2024
Department of Radiation Oncology, University Hospital of Regensburg, Franz-Josef-Strauß Allee 11, Regensburg, Germany.
There are concerns that radiotherapy for prostate cancer influences health-related quality of life in the long term. Furthermore, it is unclear whether postoperative radiotherapy is associated with a different quality of life due to a higher treatment burden compared to patients having received definitive radiotherapy for prostate cancer. This study enrolled 247 patients with localized or locally advanced prostate cancer who received external radiotherapy between 2011 and 2021.
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