Introduction: Posttraumatic stress disorder (PTSD) is a mental health disorder caused by experiencing or witnessing traumatic events. Recent studies show that patients with PTSD have an increased risk of developing dementia, including Alzheimer's disease (AD), but there is currently no way to predict which patients will go on to develop AD. The objective of this study was to identify structural and functional neural changes in patients with PTSD that may contribute to the future development of AD.
Methods: Neuroimaging (pseudo-continuous arterial spin labeling [pCASL] and structural magnetic resonance imaging [MRI]) and behavioral data for the current study ( = 67) were taken from our non-randomized open label clinical trial (ClinicalTrials.gov Identifier: NCT03229915) for treatment-seeking individuals with PTSD ( = 40) and age-matched healthy controls (HC; = 27). Only the baseline measures were utilized for this study. Mean cerebral blood flow (CBF) and gray matter (GM) volume were compared between groups. Additionally, we utilized two previously established machine learning-based algorithms, one representing AD-like brain activity (Machine learning-based AD Designation [MAD]) and the other focused on AD-like brain structural changes (AD-like Brain Structure [ABS]). MAD scores were calculated from pCASL data and ABS scores were calculated from structural T-MRI images. Correlations between neuroimaging data (regional CBF, GM volume, MAD scores, ABS scores) and PTSD symptom severity scores measured by the clinician-administered PTSD scale for DSM-5 (CAPS-5) were assessed.
Results: Decreased CBF was observed in two brain regions (left caudate/striatum and left inferior parietal lobule/middle temporal lobe) in the PTSD group, compared to the HC group. Decreased GM volume was also observed in the PTSD group in the right temporal lobe (parahippocampal gyrus, middle temporal lobe), compared to the HC group. GM volume within the right temporal lobe cluster negatively correlated with CAPS-5 scores and MAD scores in the PTSD group.
Conclusion: Results suggest that patients with PTSD with reduced GM volume in the right temporal regions (parahippocampal gyrus) experienced greater symptom severity and showed more AD-like brain activity. These results show potential for early identification of those who may be at an increased risk for future development of dementia.
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http://dx.doi.org/10.3389/fneur.2024.1470727 | DOI Listing |
Sci Rep
December 2024
School of Pharmaceutical Sciences, Siksha O Anusandhan Deemed to be University, Bhubaneswar, Odisha, India.
Diabetes mellitus is one of the metabolic syndromes that is associated with cognitive deficit, dementia, and Alzheimer's disease (AD) like pathology due to impaired insulin-signalling in the brain, oxidative stress and mitochondrial dysfunction. Nanotechnology is one of the most promising techniques for targeting the brain. However, the toxicity of metal nanoparticles is one of the biggest challenges to be studied.
View Article and Find Full Text PDFAlzheimers Res Ther
December 2024
University of Pompeu Fabra (UPF), Barcelona, Spain.
Background: Cerebrospinal fluid (CSF) biomarkers of synaptic dysfunction, neuroinflammation, and glial response, complementing Alzheimer's disease (AD) core biomarkers, have improved the pathophysiological characterization of the disease. Here, we tested the hypothesis that the co-expression of multiple CSF biomarkers will help the identification of AD-like phenotypes when biomarker positivity thresholds are not met yet.
Methods: Two hundred and seventy cognitively unimpaired adults with family history (FH) of sporadic AD (mean age = 60.
Metab Brain Dis
December 2024
Neurophysiology Research Center, Shahed University, Tehran, Iran.
Alzheimer's disease (AD) is a prevalent neurodegenerative disorder in elderly. The neurotoxicant trimethyltin (TMT) induces neurodegenerative changes, as observed in AD. The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor simvastatin (SV) has shown protective and promising therapeutic effects in neurological disorders such as AD and Parkinson's disease.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
December 2024
Department for NMR-based Structural Biology, Max Planck Institute for Multidisciplinary Sciences, Göttingen 37077, Germany.
The pathological deposition of proteins is a hallmark of several devastating neurodegenerative diseases. These pathological deposits comprise aggregates of proteins that adopt distinct structures named strains. However, the molecular factors responsible for the formation of distinct aggregate strains are unknown.
View Article and Find Full Text PDFNutrients
December 2024
Grupo de Neuropsicofarmacología, Instituto de Investigación Biomédica de Málaga y Plataforma en Nanomedicina-IBIMA Plataforma BIONAND, Unidades Clínicas de Neurología y Salud Mental, 29010 Málaga, Spain.
Background/objectives: Alzheimer's disease (AD), a leading cause of dementia, lacks effective long-term treatments. Current therapies offer temporary relief or fail to halt its progression and are often inaccessible due to cost. AD involves multiple pathological processes, including amyloid beta (Aβ) deposition, insulin resistance, tau protein hyperphosphorylation, and systemic inflammation accelerated by gut microbiota dysbiosis originating from a leaky gut.
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