We took advantage of magnetic resonance imaging (MRI) and spectroscopy (MRS) as non-invasive methods to quantify brain iron and neurometabolites, which were analyzed along with other predictors of motor dysfunction in Parkinson's disease (PD). Tapping hits, tremor amplitude, and the scores derived from part III of the Movement Disorder Society-Sponsored Revision of the Unified Parkinson Disease Rating Scale (MDS-UPDRS3 scores) were determined in 35 male PD patients and 35 controls. The iron-sensitive MRI relaxation rate R2* was measured in the globus pallidus and substantia nigra. γ-aminobutyric acid (GABA)-edited and short echo-time MRS was used for the quantification of neurometabolites in the striatum and thalamus. Associations of R2*, neurometabolites, and other factors with motor function were estimated with Spearman correlations and mixed regression models to account for repeated measurements (hands, hemispheres). In PD patients, R2* and striatal GABA correlated with MDS-UPDRS3 scores if not adjusted for age. Patients with akinetic-rigid PD subtype ( = 19) presented with lower creatine and striatal glutamate and glutamine (Glx) but elevated thalamic GABA compared to controls or mixed PD subtype. In PD patients, Glx correlated with an impaired dexterity when adjusted for covariates. Elevated myo-inositol was associated with more tapping hits and lower MDS-UPDRS3 scores. Our neuroimaging study provides evidence that motor dysfunction in PD correlates with alterations in brain iron and neurometabolites.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6406520 | PMC |
http://dx.doi.org/10.3390/cells8020096 | DOI Listing |
Sci Rep
January 2025
Department of Zoonotic Diseases, National Research Centre, Dokki, Giza, 12622, Egypt.
Toxoplasmosis induced by Toxoplasma gondii is a well-known health threat, that prompts fatal encephalitis increased with immunocompromised patients, in addition, it can cause chorioretinitis, microcephaly, stillbirth in the fetus and even led to death. Standard therapy uses sulfadiazine and pyrimethamine drugs revealed beneficial results during the acute stage, however, it has severe side effects. UPLC-ESI-MS/MS used to explore C.
View Article and Find Full Text PDFNeurochem Res
January 2025
Department of Radiology, the Second Affiliated Hospital of Kunming Medical University, No.374 Yunnan-Burma Road, Wuhua District, Kunming, Yunnan, 650101, PR China.
Objective: Post-resuscitation brain injury is a common sequela after cardiac arrest (CA). Increasing sirtuin1 (SIRT1) has been involved in neuroprotection in oxygen-glucose deprivation (OGD) neurons, and we investigated its mechanism in post-cardiopulmonary resuscitation (CPR) rat brain injury by mediating p65 deacetylation modification to mediate hippocampal neuronal ferroptosis.
Methods: Sprague-Dawley rat CA/CPR model was established and treated with Ad-SIRT1 and Ad-GFP adenovirus vectors, or Erastin.
Ferroptosis, an iron-dependent form of programmed cell death driven by oxidative stress, plays a crucial role in the progression of Alzheimer's disease (AD). Aging diminishes antioxidant systems that maintain iron homeostasis, particularly affecting the glutathione peroxidase (GPX) system, leading to increased ferroptosis and exacerbated neurodegeneration and neuroinflammation in AD. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key transcription factor regulating genes involved in antioxidant defense and ferroptosis.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Chiang Mai University/Neurophysiology Unit/Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai, Thailand.
Background: Our studies suggest that iron-overloaded rats developed neurotoxicity and cognitive impairment (1,2). An increase in brain mitochondrial fission and brain mitophagy have been considered as one of underlying mechanisms in brain with iron-overloaded condition (3,4). Hence, a pharmacological intervention focused on preventing brain mitochondrial pathologies is required.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
The University of Texas at San Antonio, San Antonio, TX, USA.
Background: Neurodegeneration is characterized by the progressive loss of neurons. However, the mechanisms by which neurons die in Alzheimer's disease (AD) remain elusive. Disrupted iron homeostasis is associated with accelerated cognitive decline, amyloid beta deposition, and AD progression, but its pathogenic relevance is poorly understood.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!