FENS-Kavli winter symposium: Addressing the cellular phase of dementia-visions of the UK Dementia Research Institute.

Christopher M Henstridge,Raphael Hesse

doi:10.1111/ejn.14059

Abstract

This is a short report summarising the plenary talk by Professor Bart de Strooper, at the 2017 FENS‐Kavli winter symposium. We have tried to capture some of the key points in his lecture on dementia research and we discuss his vision for the new UK Dementia Research Institute (UK DRI). In his talk, Prof. de Strooper encourages us to focus on the multicellular influence on brain dysfunction in dementia and we summarise how the UK DRI is a timely and ambitious, collaborative endevour, aiming to conquer dementia.

Highlights

Alzheimer’s disease (AD) is one of mankind’s greatest afflictions
To increase our understanding of the disease, generate novel therapeutic strategies and help patients suffering from dementia, a new research unit was founded in 2016: the UK Dementia Research Institute (DRI)
Bart de Strooper is the head of the UK Dementia Research Institute (UK DRI) and recently gave a plenary talk at the FENS-K avli Winter Meeting (5 December–8 December 2017) at the Institute of Science and Technology in Klosterneuburg, Austria. He opened the talk by highlighting Aβ as the culprit in AD pathogenesis, supported by the fact that all mutations in familial AD and many of the risk genes affect Aβ aggregation

Summary

Introduction

Alzheimer’s disease (AD) is one of mankind’s greatest afflictions. It is the most common degenerative illness of the human nervous system and the leading form of dementia worldwide. To increase our understanding of the disease, generate novel therapeutic strategies and help patients suffering from dementia, a new research unit was founded in 2016: the UK Dementia Research Institute (DRI). De Strooper highlighted an important point during his talk which may help us understand this, namely that PSEN1 possesses conformational flexibility which is largely influenced by single nucleotide polymorphisms (SNPs) in the PSEN1 gene (Bai, Rajendra, Yang, Shi, & Scheres, 2015).

Results

Conclusion