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PL4 Dementia as a research priority

Detailed programme, abstracts and presentations

PL4.1. The AMYPAD (Amyloid imaging to prevent Alzheimer’s disease) project: improving our understanding, diagnosis and management of Alzheimer’s disease through the utilisation of ß-amyloid PET imaging

LOPES ALVES Isadora1, GISPERT Juan Domingo2, FRISONI Giovanni3, RITCHIE Craig4, FARRAR Gill5, BARKHOF Frederik1

1VUmc, Amsterdam, The Netherlands,2Barcelonaβeta Brain Research Center, Pasqual Maragall Foundation, Barcelona, Spain,3University of Geneva, Geneva, Switzerland, 4Centre for Dementia Prevention, University of Edinburgh, Edinburgh, Uinited Kingdom, 5GE Healthcare Life Sciences, Amersham, United Kingdom

Experimental evidence supports the relationship between Alzheimer’s Disease (AD) progression and temporal changes in biomarkers such as amyloid-β (Aβ). In fact, brain Aβ accumulation appears to be one of the earliest detectable changes in progression towards AD, being therefore considered a relevant early (preclinical) AD biomarker. In this context, the Amyloid Imaging to Prevent Alzheimer’s Disease (AMYPAD) Consortium designed two clinical trials to better understand the value of Aβ PET imaging for diagnosis and patient management, as well as for risk profiling in individuals without dementia. The first, called the Diagnostic and Patient Management Study, will determine in a real-life clinical setting for whom diagnostic β‐amyloid imaging is appropriate, when this is best performed and how the resulting information is influencing diagnostic certainty, patient management and ultimately decision trees and cost‐effectiveness of dementia care. The second, derived from the European Prevention of Alzheimer’s Dementia Longitudinal Cohort Study (EPAD LCS), will quantitatively assess Aβ accumulation in a sub-set of EPAD LCS participants in order to 1) complement the ongoing phenotyping and disease modeling efforts of EPAD LCS and 2) support Proof of Concept trials by improving participant selection and treatment effect measurements using Aβ PET. Jointly, these two large European studies will provide crucial information to the clinical practice and researchers, but also to regulators, policy makers, and health care payers.

PL4.2. Importance of social and health care research in the field of Alzheimer’s disease and other dementias


Centro de Referencia Estatal de atención a personas con enfermedad de Alzheimer y otras demencias Imserso, Salamanca, España

Social and health care research in the field of dementias is essential to have a better knowledge related to the disease process of the people with dementia, but also of their caregivers.

Although this type of research has been delimited for a long time, currently its rigor is being increased, having an exceptional performance and acceptance between health and social science research.

The generation of knowledge from an social and health care approach aims to provide people with Alzheimer’s disease a better quality of healthcare, to develop new non-pharmaceutical interventions, to supply new specialised social services and resources so that the disease can be tackled. Information and communication technologies applied to Alzheimer’s disease are very important too. Therefore, psychosocial research is a crucial part of elaborating social and health care policy to deal with the necessities and search global solutions for Alzheimer’s disease and other dementias.

The results of this type of research have shown that psychosocial interventions can be as effective as medicines, and sometimes even more. The outcomes obtained form these kinds of therapies must consider participation, attitude, decision making, self-awareness and the sense of dignity of the person.

All in all, the improvement of the quality of life of the patients, the well-being of their families and the human rights of the people affected must be assessed.

It is necessary that clinical and social and health care research walk in parallel facilitating the confluence between them. This is verified as a reality thanks to the summits “Alzheimer International Madrid 2011” and “Alzheimer’s Global Summit Lisbon 2017”, supported by the National Reference Centre for Alzheimer’s and Dementia care of the IMSERSO, in which scientific evidence and progress in Alzheimer research were shown.

PL4.3. Improving the diagnosis of Alzheimer’s disease through EU research collaborations


esearch Center and Memory Clinic. Fundació ACE. Institut Català de Neurociències Aplicades, Barcelona – Universitat Internacional de Catalunya, Barcelona, Spain

There is an increasing evidence that pathological and clinical features of Alzheimer’s Disease (AD) begin many years before de phenotype of dementia shows up, giving way to the process we accept as dementia development which is moving from subjective cognitive decline, to mild cognitive impairment and then to dementia. The continuum that goes from nothing detectable to the loss of self.

To reach the optimal clinical diagnosis we must observe cognition related symptoms and functional decline or a downgrade for the normal performance. To reach the etiological diagnosis biomarkers need to be introduced.

These new scenario presents a comprehensive clinical and ethical debate focused on whether the early dementia diagnosis or predicted diagnosis is beneficial or not and how to manage it. Consequently, it is not only important regarding people’s needs, wishes and values, including their closest social and familiar environment but it should also be attentive and responsive to guaranty the chances of participating clinical trials and to ensure the ability to give their consent in advance.

PL4.4. Genetics of Alzheimer’s disease, a state-of-play

AMOUYEL Philippe

Lille University, Lille, France

Alzheimer’s disease (AD) occurrence, as for many chronic diseases, results from the interaction between environmental factors and an individual susceptibility. This susceptibility is supported by multiple variations of our genome and is usually considered to play a major role in the occurrence of AD. Less than 2% of all AD cases are primarily hereditary with early onset, affecting at least one individual in each generation. The very first genetic determinant of AD was discovered in 1991. This was a rare missense mutation located in the amyloid beta (A4) precursor protein gene (APP) segregating in a familial form of AD. Three other genes were the identified in these familial forms and were at the origin of the amyloid cascade hypothesis. For the other 98% AD sporadic late-onset cases, a family history of dementia without any specific transmission is very often registered. Since the last 10 years, the exponential progresses in the deciphering of the genome have allowed to identify more than 30 regions of the genome associated with an increased or decreased risk of AD in these late-onset forms. The main interest of this genetic information, obtained without predefined hypothesis through an agnostic screening of the whole genome, is to identify new pathophysiological pathways. These genetic researches have several consequences: an improved understanding of the molecular processes involved in AD, the identification of underlying variants that can guide us to new potential molecular targets, and a more accurate classification of patients based on these molecular approaches. Thus genetics plays a major role in our current understanding of AD and is expected to play a pivotal role in the general prevention, the identification of disruptive treatments and in the care of the disease. Indeed, due to its predictive role, genetics have a major influence on prevention, pre-symptomatic and early diagnoses of dementia that deserves a careful discussion at least for ethical considerations.

PL4.5. What pharmacological options for the treatment of behavioural symptoms of dementia


University of Exeter Medical School, Exeter, United Kingdom

Behavioral and psychological symptoms of dementia (BPSD) are nearly universal in dementia, a condition occurring in more than 40 million people worldwide. BPSD present a considerable treatment challenge for prescribers and healthcare professionals. Our recent Delphi consensus showed a clear preference for an escalating approach to the management of BPSD in AD commencing with the identification of underlying causes, caregiver training, environmental adaptations, person-centered care, and tailored activities prior to any pharmacologic approaches. If pharmacologic strategies were needed, based on current evidence citalopram and analgesia were prioritized ahead of antipsychotics for the treatment of agitation. In contrast, for psychosis, pharmacologic options, and in particular, risperidone, were prioritized following the assessment of underlying causes. Dextromethorphan/quinidine was views as a promising potential pharmacologic candidate for agitation and pimavanserin was identified as the most promising emerging treatment approach for psychosis.  A number of other new potential treatment approaches including muscarinic therapies, cannabadiol noradrenergic, and tau therapies are also beginning to emerge.  Recent work is also beginning to highlight polygenic risk and specific gene haplotypes or polymorphisms as potential tools to enable a more precision approach to treatment.




Last Updated: Wednesday 14 November 2018


  • Acknowledgements

    The 28th AE Conference in Barcelona received funding under an operating grant from the European Union’s Health Programme (2014-2020). Alzheimer Europe, CEAFA and Fundación Alzheimer España gratefully acknowledge the support of all conference sponsors.
  • European Union
  • Roche