Jennifer Imm (United Kingdom)
University of Exeter
College of Medicine and Health
Jennifer started her undergraduate degree in Biochemistry at the University of Bath in 2011, during which she undertook a year’s placement at the University of Plymouth investigating the role of mitochondrial dynamics in Parkinson’s disease. Following this she joined the Complex Disease Epigenomics group at the University of Exeter in 2015 to do her PhD under the supervision of Professor Katie Lunnon. During her PhD she characterised the epigenetic changes that occur in iPSC-neuronal and microglial models that have been exposed to Alzheimer’s disease-relevant exposures, such as differentiation and maturation, drug treatment and immune challenge. Since completing her PhD, she has continued in the Epigenomics group as a research fellow and has started a new project looking at the epigenetic changes occurring in dementia with Lewy bodies, Parkinson’s disease and Parkinson’s disease dementia using post-mortem brain samples.

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 Conference Calendar

A ROLE FOR EPIGENETIC MECHANISMS IN THE LEWY BODY DEMENTIAS

Session Name
0750 - ALPHA-SYNUCLEIN AND DISEASE MECHANISMS (ID 38)
Session Type
SYMPOSIUM
Date
Thu, 17.03.2022
Session Time
02:45 PM - 04:45 PM
Room
ONSITE: 114
Lecture Time
03:45 PM - 04:00 PM
Presenter

Abstract

Aims

The Lewy body diseases, Dementia with Lewy bodies (DLB), Parkinson’s disease (PD) and Parkinson’s disease dementia (PDD) are all neurodegenerative diseases classified by the accumulation of alpha-synuclein in neurons, forming Lewy bodies (LB). We hypothesise that these LBs cause epigenetic changes within neurons and surrounding cells and that these changes can be used to distinguish the different diseases from one another.

Methods

Bulk tissue from the cingulate gyrus and prefrontal cortex was run on the Illumina Infinium Methylation EPIC array generating a quantitative measure of DNA methylation for over 850,000 CpG sites (n=~100/disease group). Linear regression and pathway analyses were then used to identify loci that are significantly different or specific to each disease.

Results

Study groups have been sourced consisting of cases with PD, PDD and DLB based on LB deposition and clinical symptom staging. Control cases have been selected for matched age and levels of concomitant AD pathology. We have identified significant changes in methylation associated with both phenotype and neuropathology alongside the cellular pathways these changes correspond with.

Conclusions

We have collated a well powered study cohort to interrogate the epigenetic basis of neuropathological progression and clinical staging of LB disease, controlling for levels of concomitant AD pathology. We have completed bulk methylation analysis for two disease relevant brain regions and identified both phenotypic and neuropathologic changes within these regions. Processing of samples for fluorescence activated nuclei sorting has begun (n=15/group) to assess the cell type specificity of the methylation changes.

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