We aim to test whether the association between glucose control and cognitive function still holds true in elderly patients with diabetes mellitus (DM) and Alzheimer disease (AD) under health-care case management. We enrolled 100 patients with DM (mean age: 74.6 years; male: 49%) and 102 patients with AD (mean age: 77.9 years; male: 41.2%) consecutively from the Diabetes Shared Care Program and the memory clinic. These patients were followed up every 3 months with scheduled examinations. Most patients with AD were at early stage and DM was a common comorbidity (n = 42). In the DM group, there were 76 patients with subjective cognitive decline and 19 patients with mild cognitive impairment, but none sought further consultation. After adjusting for age, sex, education, and comorbidity, higher levels of glycated hemoglobin (HbA) were not associated with lower Mini-Mental State Examination (MMSE) scores in the DM group (coefficient: 0.03; 95% confidence interval [CI]: -0.44 to 0.50) and lower MMSE scores were not associated with higher HbA in the AD group either (coefficient: -0.05; 95% CI: -0.11 to 0.01). When additionally accounting for the variability of HbA in the DM group, higher standard deviation of HbA was associated with poor clock drawing test scores, but not MMSE. The coexistence of AD-DM was common, but the association between hyperglycemia and cognitive impairment was not seen in patients under regular health monitoring.
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http://dx.doi.org/10.1177/0891988718790410 | DOI Listing |
Inferior frontal sulcal hyperintensities (IFSH) observed on fluid-attenuated inversion recovery (FLAIR) MRI have been proposed as indicators of elevated cerebrospinal fluid waste accumulation in cerebral small vessel disease (CSVD). However, to validate IFSH as a reliable imaging biomarker, further replication studies are required. The objective of this study was to investigate associations between IFSH and CSVD, and their potential repercussions, i.
View Article and Find Full Text PDFJ Psychiatry Neurosci
January 2025
From the Department of Neurology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China (Qiao, Zhao, Cong, Y. Li, Tian, Yang, Cao, Su); the School of Electrical and Information Engineering, Zhengzhou University of Light Industry, Zhengzhou, China (Zhu); the Department of Medical Imaging, Henan Provincial People's Hospital & Zhengzhou University People's Hospital, Zhengzhou, China (P. Li).
Background: White matter damage is closely associated with cognitive and psychiatric symptoms and is prevalent in cerebral small vessel disease (CSVD); although the pathophysiological mechanisms involved in CSVD remain elusive, inflammation plays a crucial role. We sought to investigate the relationship between systemic inflammation markers and imaging markers of CVSD, namely white matter hyperintensity (WMH) and microstructural injury.
Methods: We conducted a study involving both cross-sectional and longitudinal data from the UK Biobank Cohort.
Prog Neuropsychopharmacol Biol Psychiatry
January 2025
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Ain Shams University, Cairo 11566, Egypt. Electronic address:
Chemotherapy-induced cognitive impairment, referred to as "chemobrain", is widely acknowledged as a significant adverse effect of cancer therapy. Paclitaxel, a chemotherapeutic drug, has been reported to cause cognitive impairment clinically and in animal models. However, the precise mechanisms are not fully understood.
View Article and Find Full Text PDFNeurotoxicology
January 2025
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Ain Shams University, Cairo, 11566, Egypt. Electronic address:
Doxorubicin (DOX)-induced chemobrain has been reported in several studies. Its main culprit is the induction of massive amounts of reactive oxygen species (ROS), hence triggering damage to brain tissues and thus leading to neuroinflammation. Biochanin A (BIO-A) is known to be an antioxidant, anti-inflammatory, and neuroprotective agent.
View Article and Find Full Text PDFBiol Psychiatry
January 2025
Translational Neuroscience Program, Department of Psychiatry, School of Medicine, University of Pittsburgh; Department of Neuroscience, Dietrich School of Arts and Sciences, University of Pittsburgh; Center for the Neural Basis of Cognition, Carnegie Mellon University. Electronic address:
Background: Certain cognitive processes require inhibition provided by the somatostatin (SST) class of gamma-aminobutyric acid (GABA) neurons in the dorsolateral prefrontal cortex (DLPFC). This inhibition onto pyramidal neuron dendrites depends on both SST and GABA signaling. Although SST mRNA levels are lower in the DLPFC in schizophrenia, it is not known if SST neurons exhibit alterations in the capacity to synthesize GABA, principally via the 67-kilodalton isoform of glutamic acid decarboxylase (GAD67).
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