Progressive myoclonus epilepsies (PMEs) represent a group of epilepsy disorders that begin in adolescence and are inherited in an autosomal recessive manner. PME patients exhibit a range of symptoms, including seizures, ataxia, muscle atrophy, dementia, psychosis, and hallucinations. The majority of these subsequent symptoms are likewise observed in older individuals, indicating the potential involvement of the PME genes in the process of aging. A recent study conducted by our group has shown that the expression of PME genes shows an inverse association with age in the normal brain. Since the stress-response mechanisms responsible for maintaining cellular homeostasis are impaired in the aging brain, we suggested that the reduction in PME gene expression may play a role in the normal aging process and the development of neurodegenerative diseases. To examine this, we used a well-known mouse model for PME, the Lafora disease (LD) mice. We conducted transcriptome sequencing on the brain tissues of LD mice and compared the expression patterns with wild-type mice brains. Our research revealed that the genes implicated in healthy brain aging follow similar expression patterns in the brains of LD mice, albeit at an accelerated pace. In addition, we have also verified expedited age-related histological and functional alterations in other vital organs, such as the liver, kidney, heart, skin, and spleen in LD mice. Our results suggest that neuropathologies in PMEs could be due to the accelerated aging process.