Related Experiment Video
Updated: May 16, 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
Accelerating cortical thinning: unique to dementia or universal in aging?
Anders M Fjell1, Lars T Westlye, Håkon Grydeland
1Research group for lifespan changes in brain and cognition, Department of Psychology, University of Oslo, 0317 Oslo, Norway.
Cerebral Cortex (New York, N.Y. : 1991)
|December 14, 2012
Summary
Accelerated cortical thinning in aging, particularly in Alzheimer's disease (AD)-vulnerable regions like the entorhinal cortex, can occur in healthy aging. This atrophy does not always indicate neurodegenerative disease and may relate to cognitive changes through non-AD mechanisms.
Area of Science:
- Neuroscience
- Gerontology
- Radiology
Background:
- Accelerated cortical atrophy, especially in Alzheimer's disease (AD)-vulnerable regions, is often associated with neurodegeneration.
- Distinguishing between pathological aging and normal aging processes is crucial for accurate diagnosis and prognosis.
Purpose of the Study:
- To investigate whether accelerated cortical atrophy in aging signifies neurodegenerative disease or is part of normal aging.
- To examine atrophy patterns in AD-vulnerable regions in healthy older adults with a very low risk of incipient AD.
Main Methods:
- Delineated age trajectories of cortical thickness cross-sectionally (n=1100) and longitudinally (n=207).
- Simulated effects of undetected AD by mixing samples.
- Examined atrophy in AD-vulnerable regions in older adults with low AD risk (stable cognition, low CSF Aβ(1-42), APOE ε4 negativity).
Main Results:
- Steady decline in cortical thickness was observed in most regions.
- Accelerated cortical thinning in the entorhinal cortex occurred across all groups, including healthy older adults.
- Entorhinal atrophy in low-risk older adults was similar to other healthy controls and predicted memory decline.
Conclusions:
- Accelerated thinning in AD-prone cortical regions does not uniquely indicate neurodegenerative illness and can be part of healthy aging.
- Non-Alzheimer's disease mechanisms in these vulnerable areas may contribute to cognitive decline observed in aging.
Related Concept Videos
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...
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...
01:30Dementia
Dementia is a collective term for cognitive disorders primarily affecting memory, thinking, and reasoning. It is not a specific disease but a syndrome, with Alzheimer's disease being the most common cause, accounting for approximately 60-80% of cases. Other types include vascular dementia, Lewy body dementia, and frontotemporal dementia. Dementia affects millions worldwide, particularly older adults, though it is not a normal part of aging.
The progression of dementia is generally gradual.
The progression of dementia is generally gradual.
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...
01:30Cognitive Development During Adulthood
Cognitive development continues throughout adulthood, undergoing significant shifts across early, middle, and late stages. Individual transition occurs from adolescent idealism to pragmatic and adaptable thinking in early adulthood. During this period, individuals learn to integrate personal beliefs with the recognition that other perspectives are equally valid. Exposure to the complexities of modern society, diverse experiences, and higher education contribute to this adaptive thought process,...
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...