Neural Regeneration Research ›› 2025, Vol. 20 ›› Issue (11): 3217-3218.doi: 10.4103/NRR.NRR-D-24-00639

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Beginning from the end: the presynaptic terminal as a pathomechanism hub in frontotemporal dementia and amyotrophic lateral sclerosis

Laura Huggon, Emma L. Clayton*   

  1. UK Dementia Research Institute at King’s College London, London, UK (Huggon L, Clayton EL) Department of Basic and Clinical Neuroscience, Institute of Psychiatry Psychology & Neuroscience, King’s College London, London, UK (Huggon L, Clayton EL)
  • Online:2025-11-15 Published:2025-02-23
  • Contact: Emma L. Clayton, PhD, emma.clayton@kcl.ac.uk.
  • Supported by:
    ELC is funded by a senior research fellowship from Alzheimer’s Research UK (ARUK-SRF2022A-005). LH is funded by a PhD studentship from Alzheimer’s Society (571). This work is supported by the UK Dementia Research Institute through UK DRI Ltd., principally funded by the UK Medical Research Council. No conflicts of interest exist between UK DRI Ltd. and publication of this article.

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Abstract: Frontotemporal dementia and amyotrophic lateral sclerosis: Frontotemporal dementia ( F T D ) a n d a m y o t r o p h i c l a t e r a l s c l e r o s i s (ALS) are neurodegenerative diseases with significant overlapping attributes. While these neurodegenerative diseases affect different neuronal populations (with FTD affecting neurons of the frontal and temporal lobes, and ALS affecting upper and lower motor neurons), these two diseases are complexly intertwined. FTD and ALS exist on a disease spectrum, with shared genetic causes, clinical presentations, and pathologies. The continuum of the genetic disease spectrum runs from those genetic mutations that cause ALS (SOD-1) through those that can cause ALS/FTD (TDP-43, FUS, CHCHD10, C9ORF72, TBK-1, UBQLN2, and CHMP2B) to those that cause FTD (MAPT and PGRN) (reviewed in Abramzon et al., 2020). Models of these genetic causes of disease have been instrumental in advancing our understanding of disease mechanisms.