Introduction: Cerebral small vessel disease (SVD) is a common accompaniment to aging. Magnetic resonance imaging (MRI) features of SVD include lacunar infarcts (LI) and white matter hyperintensity (WMH). Brain iron deposition is also a known marker of SVD that is associated with cognitive impairment and can be detected with susceptibility-weighted imaging (SWI) MRI technique. According to recent studies, the pulsation of cerebral blood flow can be one of the main factors of the development of pathological brain changes in elderly patients. The objective of this study was to investigate the relationship between the brain iron deposition, cerebral blood flow pulsation, and cognitive impairment in patients with SVD.
Materials And Methods: For the study, 97 patients with diagnosed SVD were selected. The patients were divided into two groups based on the Montreal Cognitive Assessment (MoCA) test scores. All patients underwent MRI in the SWI sequence. Pulsatility index (PI) and resistivity index (RI) were recorded from the middle cerebral artery bilaterally using transcranial Doppler (TCD).
Results: The linear regression model showed that the pulsatility index (PI) and resistivity index (RI) were associated with cognitive impairment and brain iron deposition in basal ganglia. The most significant association was found between left globus pallidus severe hypointensity voxels count and left middle cerebral artery (MCA) RI (p = 0.009).
Conclusion: The results of the study provide information that TCD indicators may be associated with brain iron deposition and cognitive decline in patients with SVD. Our findings suggest that both brain iron deposition and cerebral hemodynamics abnormalities may play an important role in the pathophysiological mechanisms of SVD.
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http://dx.doi.org/10.1007/s10072-020-04414-5 | 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.
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