Key result
Transposable elements link to neurodegenerative disorders via neuroinflammation and cytotoxicity.
Why the study?
Recent tools for evaluating transposable elements have increased appreciation for their role in human disease, motivating a summary of evidence for detrimental transposable element activity in neurodegenerative disorders.
This review highlights the emerging role of transposable elements and endogenous retroviruses in driving neuroinflammation and neurotoxicity in neurodegenerative diseases.
Endogenous retroviruses may guide biomarker or therapeutic exploration in neurodegeneration; leaves open causal validation and clinical impact.
Transposable Elements (TEs) are mobile genetic elements whose sequences constitute nearly half of the human genome. Each TE copy can be present in hundreds to thousands of locations within the genome, complicating the genetic and genomic studies of these highly repetitive sequences. The recent development of better tools for evaluating TE derived sequences in genomic studies has enabled an increasing appreciation for the contribution of TEs to human development and disease. While some TEs have contributed novel and beneficial host functions, this review will summarize the evidence for detrimental TE activity in neurodegenerative disorders. Much of the evidence for pathogenicity implicates endogenous retroviruses (ERVs), a subset of TEs that entered the genome by retroviral infections of germline cells in our evolutionary ancestors and have since been passed down as a substantial fraction of the human genome. Human specific ERVs (HERVs) represent some of the youngest ERVs in the genome, and thus are presumed to retain greater function and resultant pathogenic potential.
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Tam et al. (2019) conducted a review in Neurodegenerative diseases (AGS, MS, ALS, AD). Transposable elements and endogenous retroviruses was evaluated. Transposable elements, particularly endogenous retroviruses, are increasingly implicated in the pathogenesis of neurodegenerative disorders such as AGS, MS, ALS, and Alzheimer's disease through neuroinflammation and cytotoxicity.
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