Table 1. Genetic and epigenetic studies.

AD, Alzheimer’s dementia; CDR, Clinical Dementia Rating; MMSE, mini-mental state examination; PSG, polysomnography; SD, sleep disorder; SE, sleep efficiency; WASO, wake after sleep onset

Study	Sample characters	Methods	AD biomarkers	Results	Values
Liang et al. (2022) [18]	87 AD, 3 SD, GSE40562 dataset, 1 NC	MEGENA	Hub genes	10 hub genes related to AD and SD through neurodegeneration-related pathways
Blackman et al. (2022) [19]	96 non-ε4 carriers, 94 ε4 heterozygotes, 11 ε4 homozygotes; mean (SD) age: 84.0 (9.2), MMSE: 14.0 (11.8)	Premortem neuropsychiatry inventory scores of sleep disturbance (NPI-K) plus post-mortem histopathological findings	APOE ε4	APOE ε4 homozygosity was independently associated with sleep disturbance	Sleep disturbance was significantly associated with ε4 heterozygosity in the group without clinical dementia (CDR 0/0.5) (β 1.28, p = 0.024) and with ε4 homozygosity in the cognitively impaired group (CDR 1/2/3) (β 2.95, p = 0.045)
Yesavage et al. (2004) [20]	25 APOE ε4 carriers, 19 non-ε4 carriers; average age: 71.8 years (SD = 7.9)	6 monthly actigraph recordings and MMSE	APOE ε4	APOE status is linked with the progression of sleep/wake disturbances in AD. There is greater deterioration in negative ε4 allele than ε4 carriers in AD	Non-ε4 status (51 minutes WASO/stage; Wilcoxon signed rank test: p < 0.001) vs. APOE ε4 status (17 minutes WASO/stage; p < 0.05). SE reduction for those patients with non-ε4 status -8.6% SE/stage; p < 0.005)
Yin et al. (2016) [21]	123 newly diagnosed, drug-free AD patients, 120 matched controls; mean age: 72 ± 7 years	Sleep disturbance via PSG and blood tests	ILs, TNF-α, APOE ε4, and 31TT genotype	APOEε4 allele and IL-1β-31TT genotype led to increased IL-1β, IL-6, and TNF-α overexpression and sleep disturbance in AD patients.	APOEε4/ε4 increased the risk of AD (OR = 4.33, 95% CI = 1.33-14.10, p = 0.015)