ArticleBiomedical journal2023
Atrophy, hypometabolism and implication regarding pathology in late-life major depression with suspected non-alzheimer pathophysiology (SNAP).
Article in Biomedical journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Multiomic single-nucleus profiling reveals cell-type-specific epigenetic and transcriptional dysregulation in major depressive disorder brain.The international journal of neuropsychopharmacology · 2026Article
- Cerebral amyloid-β, glucose metabolism and hippocampal volume in major depression with and without suspected non-Alzheimer pathophysiology (SNAP).Alzheimer's research & therapy · 2025Article
- Relationships among tumor necrosis factor-alpha levels, beta-amyloid accumulation, and hippocampal atrophy in patients with late-life major depressive disorder.Brain and behavior · 2024Article
- Colonizing foreign terrain: Insights into bacterial enteropathogens.Biomedical journal · 2023Article
- The heterogeneity of late-life depression and its pathobiology: a brain network dysfunction disorder.Journal of neural transmission (Vienna, Austria : 1996) · 2023Review
- Challenges in Identifying Individualized Brain Biomarkers of Late Life Depression.Advances in geriatric medicine and research · 2023Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA substantial proportion of individuals with late-life major depression could be classified as having a suspected non-Alzheimer disease pathophysiology (SNAP), as indicated by a negative test for the biomarker β-amyloid (Aβ-) but a positive test for neurodegeneration (ND+). This study investigated the clinical features, characteristic patterns of brain atrophy and hypometabolism, and implications regarding pathology in this population.
methodsForty-six amyloid-negative patients with late-life major depressive disorder (MDD) patients, including 23 SNAP (Aβ-/ND+) and 23 Aβ-/ND- MDD subjects, and 22 Aβ-/ND-healthy control subjects were included in this study. Voxel-wise group comparisons between the SNAP MDD, Aβ-/ND- MDD and control subjects were performed, adjusting for age, gender and level of education. For exploratory comparisons, 8 Aβ+/ND- and 4 Aβ+/ND + MDD patients were included in the Supplementary Material.
resultsThe SNAP MDD patients had atrophy extending to regions outside the hippocampus, predominately in the medial temporal, dorsomedial and ventromedial prefrontal cortex; hypometabolism involving a large portion of the lateral and medial prefrontal cortex in addition to the bilateral temporal, parietal and precuneus cortex within typical Alzheimer disease regions were observed. Metabolism ratios of the inferior to the medial temporal lobe were significantly elevated in the SNAP MDD patients. We further discussed the implications with regards to underlying pathologies.
conclusionThe present study demonstrated characteristic patterns of atrophy and hypometabolism in patients with late-life major depression with SNAP. Identifying individuals with SNAP MDD may provide insights into currently unspecified neurodegenerative processes. Future refinement of neurodegeneration biomarkers is essential in order to identify potential pathological correlates while in vivo reliable pathological biomarkers are not forthcoming.
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