ArticleBrain communications2025
Cognitive and cerebral phenotypes of neurocognitive disorders due to alcohol or Alzheimer's disease.
Article in Brain communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Alcohol-Induced Dysregulation of Hydrogen Sulfide Signaling in Alzheimer's Disease-International journal of molecular sciences · 2026Review
- Recent drinking in alcohol use disorder as a modifiable risk factor of postural tremor and instability in mild cognitive impairment: An initial study.Alcohol, clinical & experimental research · 2025Article
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Distinguishing aetiologies of neurocognitive disorder (NCD) between alcohol-induced pathologies (OH) and Alzheimer's disease poses a major clinical challenge while dual diagnosis may be common. We aimed to define commonalities and specificities of neurocognitive alterations in OH or Alzheimer's Disease, considering the NCD severity (mild/major). In this retrospective cross-sectional study, we included 203 participants: 50 Mild-NCD-OH patients, 18 Major-NCD-OH patients, 30 Mild-NCD-AD patients, 24 Major-NCD-AD patients, as well as 81 healthy controls. Patients were compared on a neuropsychological and multimodal neuroimaging assessment (grey/white matter density and glucose metabolism). Analyses explored commonalities and specificities of each patient group within each NCD severity. All patient groups had episodic memory impairments, medial temporal lobe damage and hypometabolism in thalami and posteromedial cortex. NCD-AD patients had more severe cognitive deficits than NCD-OH patients, and the reverse pattern was observed for brain damage. NCD-OH patients notably showed more severe thalamic and cingulate alterations. NCD-OH patients also presented cerebellar damage not observed in NCD-AD. Volume deficits in the medial temporal lobe and memory deficits were more severe in Mild-NCD-AD than Mild-NCD-OH, but similar in Major-NCD-AD and Major-NCD-OH. Common alterations are observed in NCD-OH and NCD-AD, mainly within the memory circuit. Only cerebellar damage appears to be specific to NCD-OH. The specificity of NCD-AD deficits relies on their severity since they are also present to a lesser extent in NCD-OH, reinforcing how the neurocognitive phenotypes overlap. These results reaffirm the importance of questioning alcohol consumption in NCD-AD patients and considering an Alzheimer's Disease diagnosis in NCD-OH patients.
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