Related Experiment Video
Updated: May 11, 2026

12:21
Probing the Brain in Autism Using fMRI and Diffusion Tensor Imaging
Published on: September 12, 2011
25.1K
Alterations of White Matter Microstructure in Primary Aldosteronism Patients With Normal Cognitive Functioning Using
Weijie Chen1,2, Simin Deng3, Heng Li2
1The Second School of Clinical Medicine, Southern Medical University, Guangzhou, People's Republic of China.
International Journal of General Medicine
|March 3, 2025
Summary
Primary aldosteronism (PA) patients show early white matter microstructural changes, detected by diffusion tensor imaging (DTI), even before cognitive impairment. These findings suggest DTI can identify early biomarkers for PA-related brain changes.
Area of Science:
- Neuroimaging
- Endocrinology
- Neurology
Background:
- Primary aldosteronism (PA) is a condition linked to cardiovascular and renal issues.
- Cognitive function in PA patients is often studied, but underlying white matter changes are less understood.
- Early detection of brain alterations in PA is crucial for timely intervention.
Purpose of the Study:
- To investigate white matter microstructural alterations in primary aldosteronism (PA) patients with normal cognitive function.
- To utilize diffusion tensor imaging (DTI) to identify subtle changes in brain white matter.
- To explore potential early imaging biomarkers for PA-related neurological complications.
Main Methods:
- Recruited PA patients and healthy controls (HCs).
- Acquired T1-weighted MRI and DTI data from all participants.
- Calculated fractional anisotropy (FA), axial diffusivity (AD), radial diffusivity (RD), and mean diffusivity (MD) using the Johns Hopkins University white matter atlas.
Main Results:
- PA patients exhibited increased AD in the cingulum bundle, forceps minor, inferior fronto-occipital fasciculi, and temporo-superior longitudinal fasciculus.
- Elevated RD was observed in the left inferior fronto-occipital fasciculus and right superior longitudinal fasciculus.
- Increased MD was found in the forceps minor, bilateral inferior fronto-occipital fasciculi, and right superior longitudinal fasciculus.
Conclusions:
- Compensatory white matter alterations are present in PA patients prior to the onset of cognitive impairment.
- These DTI-derived alterations may serve as early imaging biomarkers for PA-related brain dysfunction.
- Advanced neuroimaging techniques like DTI are vital for the early diagnosis and management of PA.
Keywords:
cognitivediffusion tensor imagingprimary aldosteronismwhite matter microstructural alterationsMore Related Videos
Related Concept Videos
Alzheimer's Disease: Overview
Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
Alzheimer Disease l: Introduction
Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
Alzheimer Disease ll: Pathophysiology
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...

