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Executive function and cortical thickness in biomarker aMCI.

David M Scarisbrick^1,2,3, Cierra M Keith^1,2,3, Camila Vieira Ligo Teixeira¹

¹Rockefeller Neuroscience Institute Innovation Center Clinic, Morgantown, WV, USA.

Applied Neuropsychology. Adult

|August 14, 2024

Summary

Executive function deficits in amnestic Mild Cognitive Impairment (aMCI) worsen with amyloid presence and parietal cortex thinning. Amyloid-positive aMCI patients showed more deficits and atrophy than amyloid-negative ones.

Keywords:

AT(N)Alzheimer’s disease Go/No-Go Trail Making Test Trails B aMCI amnestic mild cognitive impairment amyloid beta-amyloid biomarker cortical thickness dementia executive function motor intrusions motor sequencing

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Area of Science:

Neuroscience
Neurology
Cognitive Science

Background:

Memory impairment is the hallmark of amnestic Mild Cognitive Impairment (aMCI).
Executive function (EF) deficits are also frequently observed in aMCI.
The influence of amyloid status and regional brain atrophy on EF in aMCI requires further investigation.

Purpose of the Study:

To investigate executive function (EF) deficits in individuals with amnestic Mild Cognitive Impairment (aMCI).
To examine the relationship between amyloid status (amyloid-positive vs. amyloid-negative) and EF deficits.
To assess the impact of regional atrophy in Alzheimer's disease (AD) signature areas on EF in aMCI.

Main Methods:

Recruited 110 individuals with aMCI (66 amyloid-positive, 44 amyloid-negative) and 33 healthy participants (HP).
Assessed executive function using four standardized neuropsychological tests.
Measured cortical thickness in AD signature brain regions via structural Magnetic Resonance Imaging (MRI).

Main Results:

Amyloid-positive (A+) aMCI participants exhibited more severe EF deficits and greater cortical atrophy in the supramarginal gyrus and superior parietal lobule compared to amyloid-negative (A-) aMCI participants.
Amyloid-negative (A-) aMCI participants showed greater EF deficits than healthy participants (HP), but without significant differences in cortical thickness within the studied AD signature areas.
Cortical thinning in parietal regions was associated with the severity of EF deficits in the aMCI group.

Conclusions:

Executive function deficits in aMCI are significantly influenced by both amyloid burden and the extent of cortical thinning in the parietal lobe.
Amyloid positivity is linked to more pronounced EF impairments and associated structural brain changes in aMCI.
These findings highlight the complex interplay between amyloid pathology, brain structure, and cognitive function in aMCI.