All the events here are relevant to people working in dementia research. If you would like to add your own you can submit an event
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Postdoc Appreciation Week at the University of Dundee
20/09/2023 @ 1:00 pm - 3:00 pm
Join us on Thursday, September 20th to celebrate National Postdoc Appreciation Week 2023 (NPAW2023) with Pint of Science and SULSA! We have three fantastic speakers lined up to talk about their research.
There will be goody bags and refreshments afterwards to encourage networking, kindly sponsored by Proteintech
#NPAW2023 #CelebratePostdocs @proteintech @pintofscience @SULSAtweets
Register to AttendBACH1 in metastasis and the tumour microenvironment
Dr David Walker (Postdoctoral Researcher)
Identifying therapies that can reduce metastasis, the growth and spread of tumour cells, is essential for increasing quality of life and survival for cancer patients. My research focuses on the transcription factor BACH1, which is highly expressed in metastatic cancers and correlates with poor prognosis and recurrence. My goal is to understand the mechanisms underlying BACH1 in metastasis with focus on its interaction with the tumour microenvironment.
Exploring the Role of VPS35 and LRRK2 in Parkinson’s Disease: Unravelling Lysosomal Connections
Dr Prosenjit Pal (Senior Research Associate ) – @Prosen21
The Parkinson’s disease-causing mutation, D620N of VPS35 gene, induces lysosomal dysfunction by enhancing LRRK2 kinase activity which alters expression of ~350 lysosomal proteins. In mouse fibroblasts, brain, and lung, we demonstrate that the VPS35 [D620N] mutation reduces RILPL1 levels, in a manner reversed by LRRK2 inhibition. Knock-out of TMEM55B increases RILPL1 levels in whole cell lysate which further confirms the link between RILPL1 and TMEM55B. Our study uncovers a pathway through which dysfunctional lysosomes resulting from the VPS35 [D620N] mutation recruit and activate LRRK2.
The mechanism of synapse loss in ALS
Dr Zsofia Laszlo (Postdoctoral Researcher)
Synapse loss is an early feature of neurodegeneration in Amyotrophic Lateral Sclerosis (ALS), affecting both the CNS and the periphery. To unfold the destructive molecular changes behind synapse dysfunction, we performed deep proteome profiling of human ALS synapses which revealed that several essential synaptic processes are disrupted and we also found key markers for glial cell recognition and phagocytosis, which could be a driving mechanism behind synapse loss.
