In numerous neurodegenerative and ND models, heterochromatin relaxation resulting in TE derepression has been documented. Some pathogenic proteins linked to ND (such as tau and TDP-43) may regulate TE expression, according to the available evidence . Inflammatory reactions to double-stranded RNA and/or cytosine nucleic acid, as well as the neurotoxic effects of retrotransposon products in amyotrophic lateral sclerosis (ALS) and Alzheimer's disease (AD) are the most prevalent pathogenic mechanisms of particular TE-derived products .