Aims: It has been suggested that in patients with type 2 diabetes mellitus (T2DM), brain atrophy is most pronounced in the hippocampus, but this has not been investigated systematically. The present pooled analysis of three studies examined if hippocampal atrophy is more prominent than global brain atrophy in patients with T2DM relative to controls.
Methods: Data were derived from a cohort study of patients with vascular disease (SMART-Medea (T2DM=120; no T2DM=502)), and from two case-control studies (UDES1 (T2DM=61; controls=30) and UDES2 (T2DM=54; controls=53)). In SMART-Medea and UDES1, hippocampal volume was obtained by manual tracing on 1.5 Tesla (T) MRI scans. Total brain and intracranial volume (ICV) were determined by an automated segmentation method. In UDES2, hippocampal and total brain volume were determined by FreeSurfer and ICV by manual segmentation on 3 T MRI scans.
Results: The pooled analyses, adjusted for age and sex, showed a significant negative relation between T2DM and total brain-to-ICV ratio (standardized mean difference=-1.24%, 95% CI: -1.63; -0.86), but not between T2DM and hippocampal-to-ICV ratio (0.00%, 95% CI: -0.01; 0.00) or between T2DM and hippocampal-to-total brain volume ratio (0.01%, 95% CI: -0.01; 0.02). In patients with T2DM no associations were found between brain volume measures and HbA1c or memory.
Conclusion: Patients with T2DM had greater brain atrophy but not hippocampal atrophy, compared to controls. These findings do not support specific vulnerability of the hippocampus in patients with T2DM.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.jns.2014.06.008 | DOI Listing |
Hum Brain Mapp
February 2025
Department of Neurology, Washington University in St. Louis, St. Louis, Missouri, USA.
Neurodegeneration is presumed to be the pathological process measure most proximal to clinical symptom onset in Alzheimer Disease (AD). Structural MRI is routinely collected in research and clinical trial settings. Several quantitative MRI-based measures of atrophy have been proposed, but their low correspondence with each other has been previously documented.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Innovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, National Clinical Research Center for Geriatric Diseases, Xicheng District, Beijing, China.
Alzheimer's disease (AD) is a degenerative disease characterized by progressive cognitive dysfunction. The strong link between nutrition and the occurrence and progression of AD pathology has been well documented. Poor nutritional status accelerates AD progress by potentially aggravating amyloid beta (Aβ) and tau deposition, exacerbating oxidative stress response, modulating the microbiota-gut-brain axis, and disrupting blood-brain barrier function.
View Article and Find Full Text PDFTemporal lobe epilepsy with hippocampal sclerosis (TLE-HS) is associated with a complex genetic architecture, but the translation from genetic risk factors to brain vulnerability remains unclear. Here, we examined associations between epilepsy-related polygenic risk scores for HS (PRS-HS) and brain structure in a large sample of neurotypical children, and correlated these signatures with case-control findings in in multicentric cohorts of patients with TLE-HS. Imaging-genetic analyses revealed PRS-related cortical thinning in temporo-parietal and fronto-central regions, strongly anchored to distinct functional and structural network epicentres.
View Article and Find Full Text PDFStudy Objectives: Sleep deficiency is associated with Alzheimer's disease (AD) pathogenesis. We examined the association of sleep architecture with anatomical features observed in AD: (1) atrophy of hippocampus, entorhinal, inferior parietal, parahippocampal, precuneus, and cuneus regions ("AD-vulnerable regions") and (2) cerebral microbleeds.
Methods: In 271 participants of the Atherosclerosis Risk in the Communities Study, we examined the association of baseline sleep architecture with anatomical features identified on brain MRI 13∼17 years later.
Tremor Other Hyperkinet Mov (N Y)
January 2025
Department of Neurology, Medical University of Graz, Graz, Austria.
Background: Ataxia-telangiectasia (Louis-Bar syndrome) is a rare genetic disorder characterized by progressive ataxia, ocular telangiectasias, immunodeficiency and increased cancer risk due to impaired DNA repair.
Phenomenology Shown: Thorough clinical and subsequently radiological examination in a 19-year-old woman with a history of previously undiagnosed, progressive gait ataxia since early childhood, diffuse large B-cell lymphoma and severe combined immunodeficiency revealed the eponymous features of the disease, ocular telangiectasias and cerebellar atrophy, enabling targeted genetic testing.
Educational Value: Ocular telangiectasias represent an important clue for a diagnosis of ataxia-telangiectasia in young patients with progressive ataxia, implicating awareness of increased malignancy risk and treatment of immunodeficiency.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!