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Background: Diabetic cognitive dysfunction (DCD) is one of the most insidious complications of type 2 diabetes mellitus, which can seriously affect the ability to self-monitoring of blood glucose and the quality of life in the elderly. Previous pathological studies of cognitive dysfunction have focused on neuronal dysfunction, characterized by extracellular beta-amyloid deposition and intracellular tau hyperphosphorylation. In recent years, astrocytes have been recognized as a potential therapeutic target for cognitive dysfunction and important participants in the central control of metabolism. The disorder of gut microbiota and their metabolites have been linked to a series of metabolic diseases such as diabetes mellitus. The imbalance of intestinal flora has the effect of promoting the occurrence and deterioration of several diabetes-related complications. Gut microbes and their metabolites can drive astrocyte activation.
Aims: We reviewed the pathological progress of DCD related to the "gut microbiota-astrocyte" axis in terms of peripheral and central inflammation, intestinal and blood-brain barrier (BBB) dysfunction, systemic and brain energy metabolism disorders to deepen the pathological research progress of DCD and explore the potential therapeutic targets.
Conclusion: "Gut microbiota-astrocyte" axis, unique bidirectional crosstalk in the brain-gut axis, mediates the intermediate pathological process of neurocognitive dysfunction secondary to metabolic disorders in diabetes mellitus.
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http://dx.doi.org/10.1111/cns.14077 | DOI Listing |
Alzheimers Dement
September 2025
Department of Neurology, University of Michigan, Ann Arbor, Michigan, USA.
Introduction: Mild cognitive impairment (MCI) represents a transitional stage between normal aging and dementia. We investigate associations among cardiovascular and metabolic disorders (hypertension, diabetes mellitus, and hyperlipidemia) and diagnosis (normal; amnestic [aMCI]; and non-amnestic [naMCI]).
Methods: Multinomial logistic regressions of participant data (N = 8737; age = 70.
J Mol Neurosci
September 2025
Department of Physiology, School of Medicine, Dokuz Eylul University, Izmir, Turkey.
The ketogenic diet (KD), a high-fat, low-carbohydrate regimen, has been shown to exert neuroprotective effects in various neurological models. This study explored how KD-alone or combined with antibiotic-induced gut microbiota depletion-affects cognition and neuroinflammation in aging. Thirty-two male rats (22 months old) were assigned to four groups (n = 8): control diet (CD), ketogenic diet (KD), antibiotics with control diet (AB), and antibiotics with KD (KDAB).
View Article and Find Full Text PDFSci Rep
September 2025
Department of Endocrinology, Affiliated Zhongda Hospital of Southeast University, Nanjing, China.
Visceral adiposity has been proposed to be closely linked to cognitive impairment. This cross-sectional study aimed to evaluate the predictive value of Chinese Visceral Adiposity Index (CVAI) for mild cognitive impairment (MCI) in patients with type 2 diabetes mellitus (T2DM) and to develop a quantitative risk assessment model. A total of 337 hospitalized patients with T2DM were included and randomly assigned to a training cohort (70%, n = 236) and a validation cohort (30%, n = 101).
View Article and Find Full Text PDFPsychogeriatrics
September 2025
Department of Psychiatry, The 4th People's Hospital of Ziyang, Ziyang Psychosis Hospital, Ziyang, China.
Background: Olfactory training (OT) has been proposed as a non-pharmacological intervention to improve cognitive functions and depressive symptomatology, but evidence remains fragmented.
Methods: In this study, we conducted a systematic review and meta-analysis of randomised controlled trials (RCTs) comparing OT versus control in middle-aged and elderly adults. Four databases (PubMed, Cochrane Library, Web of Science, Embase) were systematically searched from database inception through June 2025.
Cell Rep
September 2025
Department of Neurology, University of California, Los Angeles, David Geffen School of Medicine, Los Angeles, CA 90095, USA; Department of Neurobiology, University of California, Los Angeles, Los Angeles, CA 90095, USA; Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research, Un
Neurodevelopmental disorders often impair multiple cognitive domains. For instance, a genetic epilepsy syndrome might cause seizures due to cortical hyperexcitability and present with memory impairments arising from hippocampal dysfunction. This study examines how a single disorder differentially affects distinct brain regions using induced pluripotent stem cell (iPSC)-derived cortical- and hippocampal-ganglionic eminence assembloids to model developmental and epileptic encephalopathy 13, a condition arising from gain-of-function mutations in the SCN8A gene encoding the sodium channel Nav1.
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