Cognitive Impairment in Late-Onset Psychotic Disorders

Late-onset psychotic disorders, defined by first presentation of non-affective psychosis at or beyond the sixth decade of life, challenge traditional boundaries between primary psychiatric illness and neurodegenerative disease. Cognitive deficits in this population encompass impairments in memory, executive function, attention and processing speed, often resembling early stages of dementia yet retaining distinct clinical trajectories. Structural neuroimaging studies report hippocampal and thalamic volume reductions that differ in pattern and magnitude from those seen in Alzheimer’s disease. Biomarker investigations reveal that a subset of individuals with very late-onset schizophrenia-like psychosis harbour elevated phosphorylated tau or amyloid-β pathology, suggesting overlapping pathological substrates in some cases. Epidemiological analyses underscore a substantially increased risk of subsequent dementia in those with late-onset psychosis, prompting reconsideration of diagnostic criteria and longitudinal management strategies. Emerging evidence highlights genetic contributions and psychosocial factors—such as sensory impairment and social isolation—that modulate cognitive reserve and functional outcome. The global burden of cognitive deterioration in late-onset psychosis calls for integrated assessment protocols combining neuropsychological testing, imaging and biochemical markers, with a view to personalised intervention and monitoring for neurodegenerative progression.

Research from Nature Portfolio

No recent Nature Portfolio content available.

Cognitive Impairment in Late-Onset Psychotic Disorders publication trend

The graph below shows the total number of articles in cognitive impairment in late-onset psychotic disorders across all publications each year (not limited to Nature Index journals).

Technical terms

Very late-onset schizophrenia-like psychosis (VLOSLP): A schizophrenia spectrum disorder with first psychotic episode at age 60 or older.

Dementia: A syndrome characterised by progressive decline in cognitive function severe enough to impair daily activities.

Biomarker: A measurable indicator of a biological state, such as phosphorylated tau or amyloid-β levels in cerebrospinal fluid or PET imaging.

Hippocampal atrophy: Reduction in hippocampal volume, often measured by MRI and associated with memory impairment.

Amyloid-β: A protein fragment that accumulates in Alzheimer’s disease and may be detected by PET or in cerebrospinal fluid.

Phosphorylated tau: A modified form of the tau protein that aggregates in neurofibrillary tangles and serves as a marker of neurodegeneration.

References

1. Genetic overlap between schizophrenia spectrum disorders and Alzheimer's disease: Current evidence and future directions – An integrative review. Neuroscience & Biobehavioral Reviews (2024).
2. Biomarkers of neurodegeneration in schizophrenia: systematic review and meta-analysis. BMJ Mental Health (2024).
3. Subcortical Structures in Demented Schizophrenia Patients: A Comparative Study. Biomedicines (2023).
4. Association between risk of dementia and very late-onset schizophrenia-like psychosis: a Swedish population-based cohort study. Psychological Medicine (2021).
5. Characteristics of very late-onset schizophrenia-like psychosis classified with the biomarkers for Alzheimer’s disease: a retrospective cross-sectional study. International Psychogeriatrics (2023).
6. Non-affective psychotic disorders and risk of dementia: a systematic review and meta-analysis. Psychological Medicine (2022).
7. Cognitive impairment and development of dementia in very late-onset schizophrenia-like psychosis: a systematic review. Irish Journal of Psychological Medicine (2021).