Behavioral and dysexecutive variant of Alzheimer’s disease: Insights from structural and molecular imaging studies

1. Heliyon. 2024 Apr 9;10(8):e29420. doi: 10.1016/j.heliyon.2024.e29420.
eCollection 2024 Apr 30.

Behavioral and dysexecutive variant of Alzheimer’s disease: Insights from
structural and molecular imaging studies.

Nabizadeh F(1)(2), Pirahesh K(3), Aarabi MH(4), Wennberg A(5), Pini L(4).

Author information:
(1)School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
(2)Neuroscience Research Group (NRG), Universal Scientific Education and
Research Network (USERN), Tehran, Iran.
(3)School of Medicine, Tehran University of Medical Science, Tehran, Iran.
(4)Padova Neuroscience Center, University of Padova, Italy.
(5)Department of Clinical Neuroscience, Karolinska Institutet, Stockholm,
Sweden.

Frontal variant Alzheimer’s disease (AD) manifests with either behavioral or
dysexecutive syndromes. Recent efforts to gain a deeper understanding of this
phenotype have led to a re-conceptualization of frontal AD. Behavioral (bAD) and
dysexecutive (dAD) phenotypes could be considered subtypes, as suggested by both
clinical and neuroimaging studies. In this review, we focused on imaging studies
to highlight specific brain patterns in these two uncommon clinical AD
phenotypes. Although studies did not compare directly these two variants, a
common epicenter located in the frontal cortex could be inferred. On the
contrary, 18F-FDG-PET findings suggested differing metabolic patterns, with bAD
showing specific involvement of frontal regions and dAD exhibiting widespread
alterations. Structural MRI findings confirmed this pattern, suggesting that
degeneration might involve neural circuits associated with behavioral control in
bAD and attentional networks in dAD. Furthermore, molecular imaging has
identified different neocortical tau distribution in bAD and dAD patients
compared to typical AD patients, although the distribution is remarkably
heterogeneous. In contrast, Aβ deposition patterns are less differentiated
between these atypical variants and typical AD. Although preliminary, these
findings underscore the complexity of AD frontal phenotypes and suggest that
they represent distinct entities. Further research is essential to refine our
understanding of the pathophysiological mechanisms in frontal AD.

© 2024 The Author(s).

DOI: 10.1016/j.heliyon.2024.e29420
PMCID: PMC11024599
PMID: 38638964

Conflict of interest statement: The authors declare that they have no known
competing financial interests or personal relationships that could have appeared
to influence the work reported in this paper.

Auteurs Bordeaux Neurocampus