Journal of affective disorders · 2026
Cortical β-amyloid deposition and cognitive impairment in remitted late-onset depression: An [18F]Florbetapir PET study.
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Jiang Fugui, Yi Yang, Zhang Jing, Tan Arui, Qin Xiaohong, Zhong Xuemei, Wang Peijia, Xiao Jun, Zhou Bo, Li Jieying
Аннотация
BACKGROUND: Late-onset depression (LOD) has been associated with increased risk of Alzheimer's disease (AD), but amyloid-β (Aβ) abnormalities may not be uniformly present across all clinical subtypes. This study examined cortical Aβ deposition in remitted LOD (RLOD) patients with and without cognitive impairment to clarify heterogeneity in AD-related pathology.
METHODS: Eighty participants were enrolled, including 30 cognitively impaired RLOD (RLOD-CI), 30 cognitively unimpaired RLOD (RLOD-CU), and 20 healthy controls (HC). All underwent [^18F]Florbetapir PET imaging, with global Aβ positivity defined as SUVR ≥1.10. Regional SUVR values were quantified using the AAL3 atlas. Episodic memory performance was normalized using Z-scores derived from the HC group. Group differences and correlation analyses were performed with appropriate statistical corrections.
RESULTS: RLOD-CI patients showed significantly elevated Aβ burden in multiple cortical regions-including the frontal, temporal, parietal, occipital, cingulate, precuneus and global cortices-compared with HC and RLOD-CU (all p < 0.05). Aβ positivity rates were 66.7 % (RLOD-CI), 36.7 % (RLOD-CU), and 35.0 % (HC). Within the RLOD-CI group, frontal SUVRs were negatively correlated with immediate (r = -0.48, p = 0.0067) and delayed (r = -0.42, p = 0.022) memory Z-scores, while no other cognitive domains showed significant associations.
CONCLUSIONS: Aβ deposition is selectively increased in cognitively impaired-but not cognitively unimpaired-RLOD patients, supporting RLOD-CI as a distinct phenotype potentially reflecting prodromal AD. The modest association between frontal Aβ burden and episodic memory further underscores heterogeneity within LOD. Longitudinal studies are warranted to clarify progression risk and evaluate the predictive value of Aβ imaging in this population.
METHODS: Eighty participants were enrolled, including 30 cognitively impaired RLOD (RLOD-CI), 30 cognitively unimpaired RLOD (RLOD-CU), and 20 healthy controls (HC). All underwent [^18F]Florbetapir PET imaging, with global Aβ positivity defined as SUVR ≥1.10. Regional SUVR values were quantified using the AAL3 atlas. Episodic memory performance was normalized using Z-scores derived from the HC group. Group differences and correlation analyses were performed with appropriate statistical corrections.
RESULTS: RLOD-CI patients showed significantly elevated Aβ burden in multiple cortical regions-including the frontal, temporal, parietal, occipital, cingulate, precuneus and global cortices-compared with HC and RLOD-CU (all p < 0.05). Aβ positivity rates were 66.7 % (RLOD-CI), 36.7 % (RLOD-CU), and 35.0 % (HC). Within the RLOD-CI group, frontal SUVRs were negatively correlated with immediate (r = -0.48, p = 0.0067) and delayed (r = -0.42, p = 0.022) memory Z-scores, while no other cognitive domains showed significant associations.
CONCLUSIONS: Aβ deposition is selectively increased in cognitively impaired-but not cognitively unimpaired-RLOD patients, supporting RLOD-CI as a distinct phenotype potentially reflecting prodromal AD. The modest association between frontal Aβ burden and episodic memory further underscores heterogeneity within LOD. Longitudinal studies are warranted to clarify progression risk and evaluate the predictive value of Aβ imaging in this population.