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Review

Epigenetic regulatory modifications in genetic and sporadic frontotemporal dementia

ORCID Icon, ORCID Icon & ORCID Icon
Pages 469-475 | Received 13 Feb 2018, Accepted 23 May 2018, Published online: 05 Jun 2018
 

ABSTRACT

Introduction: Epigenetic modifications have recently been linked to neurodegenerative diseases, such as frontotemporal dementia (FTD), which represents the second most common form of dementia in adulthood after Alzheimer’s disease (AD). Epigenetic regulation occurs at different cellular levels and serve as a way to alter genetic information not only in aging but also following environmental signals. Thus, epigenetics mechanisms could exert their function at early stage of the disease, especially in sporadic cases.

Areas covered: Herein, the available evidence supporting the concept that epigenetic-driven changes might shed the light into the pathogenic mechanisms of FTD will be summarized, with particular regard to their influence in underlying sporadic/familiar FTD onset and/or severity, and to the possibility to open a new scenario to facilitate early diagnosis and the identification of novel therapeutic targets. Bibliographic search through PubMed was used to find the studies included in this review.

Expert commentary: Although epigenetic investigation in neurodegenerative disorders is in its infancy, recent advances in the technology of epigenetic change determination has led to novel, challenging findings. In particular, the knowledge and the characterization of epigenetic events could result in novel therapeutic strategies.

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This work was supported by grants from the Italian Ministry of Health [NET-2011-02346784] and the Monzino Foundation.

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