Related Experiment Video
Updated: Aug 2, 2026
09:57
How to Measure Cortical Folding from MR Images: a Step-by-Step Tutorial to Compute Local Gyrification Index
Published on: January 2, 2012
Late-life depression and microstructural abnormalities in dorsolateral prefrontal cortex white matter
Warren D Taylor1, James R MacFall, Martha E Payne
1Department of Psychiatry, Duke University Medical Center, DUMC Box 3903, Durham, NC 277120, USA. Taylo066@mc.duke.edu
The American Journal of Psychiatry
|July 2, 2004
Summary
Late-life depression is linked to white matter changes in the brain. Specifically, lower fractional anisotropy in the right superior frontal gyrus was observed in depressed elderly individuals.
Area of Science:
- Neuroimaging
- Geriatric Psychiatry
- Neuroscience
Background:
- Late-life depression is a significant public health concern.
- The underlying neurobiological mechanisms of late-life depression are not fully understood.
- White matter integrity may play a role in cognitive function and mood regulation in older adults.
Purpose of the Study:
- To investigate the association between white matter microstructural abnormalities in the dorsolateral prefrontal cortex and late-life depression.
- To determine if diffusion tensor imaging (DTI) can detect these abnormalities.
Main Methods:
- Diffusion tensor imaging (DTI) was employed to assess white matter integrity.
- Fractional anisotropy (FA) was measured in the superior and middle frontal gyri of the dorsolateral prefrontal cortex (DLPFC) and the left occipital lobe (control).
- Seventeen elderly depressed subjects were compared with 16 non-depressed elderly controls, with adjustments for age, sex, and medical comorbidities.
Main Results:
- Significantly lower fractional anisotropy (FA) values were found in the white matter of the right superior frontal gyrus in depressed elderly subjects compared to controls.
- These findings remained significant after controlling for age, sex, hypertension, and heart disease.
- No significant differences were observed in the other measured white matter regions.
Conclusions:
- Microstructural white matter changes in the right superior frontal gyrus are associated with late-life depression.
- These findings suggest a potential neurobiological marker for late-life depression.
- Further research is warranted to elucidate the functional implications of these white matter alterations in depression.
Related Concept Videos
01:05Long-term Depression
Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
01:03Long-term Depression
Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
If over time, all...
Calcium Ion Concentration Mechanism
If over time, all...
01:26Alzheimer'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...
01:29Alzheimer 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...
01:23Alzheimer 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...
01:22Dementia l: Introduction
Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...