AbstractBackgroundThe Lewy body diseases (LBDs), Dementia with Lewy bodies (DLB), Parkinson’s disease (PD) and Parkinson’s disease dementia (PDD) are all neurodegenerative diseases classified by the accumulation of alpha‐synuclein in neurons, forming Lewy bodies (LBs). As both the LBDs and the shortening of telomeres are well established with aging it is reasonable to hypothesise some involvement of telomere shortening in the LBDs. There are few studies addressing telomere length changes in the LBDs and as these studies are often conflicting, we aim to rectify this disparity and establish whether there is a relationship between disease diagnosis, LB Braak staging and epigenetic age.MethodBulk cingulate gyrus and prefrontal cortex tissue was used to determine absolute telomere length using quantitative real‐time PCR. Alongside sample DNA, standards for either telomeric repeats or a housekeeping gene, ribosomal phosphoprotein P0 (36B4), for which the copy number was known were run. Calculation of absolute telomere length was achieved by dividing the telomere copies per reaction by the corresponding 36B4 copies per reaction. This value was then further divided by 92 to give the length per individual telomere. Linear regression was used to determine significance within each brain region controlling for age, gender and cellular composition. DNA methylation was assessed using the Illumina EPIC array and epigenetic age was derived using the Horvath skin and blood clock.ResultWe have used 136 PD, 307 PDD, 178 DLB and 302 control samples in two different brain regions in order to determine the relationship between telomere length, epigenetic age, neuropathology and clinical diagnosis.ConclusionWe have studied how telomere length varies not only in relation to epigenetic age in post‐mortem brain samples but also how it relates to clinical diagnosis and neuropathology in the LBDs.