| 1. |
- Henshall, David C., et al.
(författare)
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Shaping the future of European epilepsy research : Final meeting report from EPICLUSTER
- 2023
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Ingår i: Epilepsy Research. - : Elsevier BV. - 0920-1211. ; 189
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Tidskriftsartikel (refereegranskat)abstract
- Collaboration is essential to the conduct of basic, applied and clinical research and its translation into the technologies and treatments urgently needed to improve the lives of people living with brain diseases and the health professionals who care for them. EPICLUSTER was formed in 2019 by the European Brain Research Area (EBRA) to support the coordination of epilepsy research in Europe. A key objective was to provide a platform to discuss shared research priorities by bringing together scientists and clinicians with multiple stakeholders including patient organisations and industry and the networks and infrastructures that provide healthcare and support research. Additional objectives were to facilitate access and sharing of data and biosamples, working together to ensure epilepsy is a priority for research funding, and embedding a culture of public and patient involvement (PPI) among epilepsy researchers. In this meeting report, we summarise the shared research priorities discussed by the leadership of EPICLUSTER at the recent final meeting. We also briefly review the discussion on patient and industry priorities, guidance on starting PPI for epilepsy researchers, and the sustainability of funding and infrastructures needed to ensure a comprehensive stakeholder-embedded community for epilepsy research.
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| 2. |
- Lerche, Stefanie, et al.
(författare)
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Cognitive impairment in Glucocerebrosidase (GBA)-associated PD: Not primarily associated with cerebrospinal fluid Abeta and Tau profiles.
- 2017
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Ingår i: Movement disorders : official journal of the Movement Disorder Society. - : Wiley. - 1531-8257. ; 32:12
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Tidskriftsartikel (refereegranskat)abstract
- A proportion of idiopathic Parkinson's disease patients (PDidiopathic ) with dementia show altered CSF profiles of amyloid β (Aβ) and Tau. PD patients with Glucocerebrosidase (GBA) mutations (PDGBA ) present with even more cognitive decline than seen in PDidiopathic .The objective of this study was to evaluate whether CSF profiles of Aβ and tau are associated with the prominent cognitive impairment in PDGBA .CSF levels of Aβ1-42 , t-Tau, p-Tau, and total alpha-synuclein were assessed in 479 participants (50 PDGBA , 308 PDidiopathic , 121 healthy controls).Older age was associated with cognitive impairment in PDGBA and PDidiopathic . Despite prominent cognitive impairment, PDGBA showed similar CSF levels of Aβ1-42 , t-Tau, and p-Tau as seen in healthy controls. In contrast, lower levels of Aβ1-42 and higher levels of t-Tau and p-Tau were associated with worse cognitive performance in PDidiopathic .The prominent cognitive impairment in PDGBA seems not primarily associated with Aβ and Tau profiles in CSF. © 2017 International Parkinson and Movement Disorder Society.
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| 3. |
- Lerche, Stefanie, et al.
(författare)
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Parkinson's disease : Evolution of cognitive impairment and CSF Aβ1-42 profiles in a prospective longitudinal study
- 2019
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Ingår i: Journal of Neurology, Neurosurgery and Psychiatry. - : BMJ. - 0022-3050 .- 1468-330X. ; 90:2, s. 165-170
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Tidskriftsartikel (refereegranskat)abstract
- Objective: To evaluate the evolution of cognitive impairment in relation to cerebrospinal fluid (CSF) profiles of amyloid-β (Aβ), total-Tau and phosphorylated-Tau in Parkinson's disease (PD). Methods: Prospective, longitudinal, observational study up to 10 years with follow-up every 2 years. We assessed CSF profiles in 415 patients with sporadic PD (median age 66; 63% men) and 142 healthy controls (median age 62; 43% men). Results: Patients with PD with low CSF Aβ1-42 levels at baseline were more often cognitively impaired than patients with intermediate and high Aβ1-42 levels. Sixty-seven per cent of the patients with low Aβ1-42 levels at baseline and normal cognition developed cognitive impairment during follow-up, compared with 41% and 37% of patients having intermediate and high CSF Aβ1-42 levels. Kaplan-Meier survival curves and Cox regression revealed that patients with low CSF Aβ1-42 levels at baseline developed cognitive impairment more frequently and earlier during follow-up. Conclusion: We conclude that in patients with sporadic PD, low levels of Aβ1-42 are associated with a higher risk of developing cognitive impairment earlier in the disease process at least in a subgroup of patients.
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