Sleep disturbances are increasingly recognized as early and clinically meaningful features in the pathophysiology of neurodegenerative diseases. Polysomnography (PSG), i.e., the gold standard for objectively characterizing sleep architecture, may provide non-invasive and scalable biomarkers for both early detection and differential diagnosis of dementia. This systematic review and network meta-analysis aims to synthesize existing evidence on PSG-derived sleep alterations across the neurodegenerative continuum, including subjective cognitive impairment, mild cognitive impairment, Alzheimer’s disease, frontotemporal dementia, Lewy body dementia, and Parkinson’s disease dementia, compared to healthy controls. It will adhere to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines for reporting systematic reviews that include network meta-analyses, and it has been registered with the International Prospective Register of Systematic Reviews (PROSPERO) under registration number CRD420251114418. We will include peer-reviewed studies with nocturnal PSG data from adult participants, categorized using validated diagnostic criteria, and scored according to the most recent American Academy of Sleep Medicine guidelines. Both pairwise and network meta-analyses will be conducted using standardized mean differences to quantify group-level effects. Additional analyses will explore the correlations between PSG parameters, severity of cognitive impairment, behavioral symptoms, treatments, and relevant comorbidities. Longitudinal data, where available, will be analyzed separately to evaluate prognostic value. This study will provide a comprehensive synthesis of PSG alterations across neurodegenerative disorders, offering insights into their diagnostic utility and potential as early markers for stratification in clinical trials of disease-modifying therapies.

Isolated rapid-eye-movement sleep behaviour disorder (RBD) is considered the prodromal stage of α-synucleinopathies (e.g., Parkinson’s disease and dementia with Lewy bodies); however, iRBD patients show a wide variety in the progression timing (5–15 years). The model of cognitive reserve (CR) might contribute to explaining this phenomenon. Our exploratory study aimed to evaluate, for the first time, the impact of CR level on cognitive performance in polysomnography-confirmed iRBD patients. Fifty-five iRBD patients (mean age ± SD: 66.38 ± 7.51; M/F 44/11) underwent clinical and neuropsychological evaluations at the time of diagnosis. The CR Index questionnaire was part of the clinical assessment. We found that iRBD patients with high levels of CR showed: (i) the lowest percentage of mild cognitive impairment (10%), and (ii) the best performance in visuo-constructive and verbal memory functions (i.e., the recall of the Rey–Osterrieth complex figure test). Our results suggest that CR might help iRBD patients better cope with the cognitive decline related to the neurodegenerative process, providing the first preliminary findings supporting CR as a possible protective factor in this condition. This might pave the way for future longitudinal studies to evaluate the role of CR as a modulating factor in the timing of iRBD conversion and cognitive deterioration development.