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Spillantini Lab


Person, Project, Place

Break-through research needs talented enthusiastic scientists, matched to well designed projects, in a supportive place. The Spillantini lab has a long history of attracting postdoctoral researchers and PhD students from around the world. Many have gone on to start their own lab and purse independent research careers. Others have moved into industry or successful consulting roles. You can find the profiles of current members below.

Want to join?

Do you think you have  a novel research idea? Do you have the drive to win funding? Do you want to perform world-class research at the University of Cambridge? Then please contact us to book an appointment. Call +44 (0)1223 331160 or email


Postdoctoral Research Associates 




Dr Jack Harry Brelstaff (
I investigate how and why neurons die in dementia. Some neurodegenerative diseases are caused by the protein tau aggregating inside the neuron. These include Alzheimer’s disease, Frontotemporal dementia (FTD-17P), Progressive Supranuclear Palsy (PSP), Cortical Basal Degeneration (CBD) and even chronic traumatic encephalopathy (punch drunk syndrome).  But no one knows for sure how the aggregate of tau kills the neuron. My research points to a communication between the sick neuron and the immune system, causing it to remove the neuron much like it would a cell infected with a virus. The problem is that this cell is still alive and part of the brain network, but once the immune system removes it, it's gone forever. Then the immune cell has to deal with the aggregate of tau, which is difficult to destroy. New evidence suggests that as the immune cell chips away at the aggregate, it releases fragments that are dangerous and can cause more aggregation elsewhere. 

  • ARUK junior fellow; Research Associate Fellow of Clare College; Supervisor to Natural Science students at Clare College

Image: A slice through a brain showing all the aggregated tau causing degeneration in green. pFTAA labelled P301S human tau aggregates



Dr Laura Calo (
Neurons communicate to one another via synapses which is where the signal jumps from one neuron to the next. In Parkinson's disease (PD) the synaptic protein alpha synuclein aggregates and spreads to the connected neurons via synapses, eventually killing the neurons. My research aims to understand the mechanisms that lead to synaptic dysfunction and alpha-synuclein aggregation. I do this by growing neurons from induced pluripotent stem cells derived from skin biopsies taken from PD patients. My aim is to identify and test potential therapeutics that inhibit aggregation and transmission of alpha-synuclein in an effort to stop or delay the loss of neurons in PD and other synucleopathies.

  • Darwin College Cambridge alumna

Image: Neurons derived from a skin biopsy of a PD case showing alpha synuclein aggregation in green (puncta)


Dr Ellen Tedford (

I am interested in the role extracellular vesicles play in neurodegenerative diseases. Extracellular vesicles are shed by almost every cell type, including neurons and glia, they contain RNA, DNA and protein. This is an important part of neurophysiological communication but during neurodegenerative diseases this process is altered. To investigate the mechanisms governing this dysfunction I use human iPS cells and animal models. During my PhD, I investigated the role extracellular vesicles play in epigenetic regulation of neurons.

  • UNIVERSITY OF LEEDS, PhD 2018; MSc 2014; BSc 2013


Dr Sanne Kaalund 
My current research relates the macroscopic structural and functional changes caused by frontotemporal lobar degeneration as seen on brain scans like MRI, to the microscopic changes such as the highly selective loss of neurons by region, cortical layer and cell type.  Leading up to this work, in my PhD and previous postdoctoral position in Copenhagen, I specialized in stereology for quantifying cell numbers, volumes and surface areas, in combination with functional outputs such as motor and cognitive behavior in rodent and porcine models. Together with Professor Bente Pakkenberg and Dr. Mikkel Olesen I co-edited a Frontiers of Neuroanatomy special issue on “Neurostereology” . A  parallel  line of my research concerns genetic and gene-expression variation in neuropsychiatric disorders such as  schizophrenia. 

  • UNIVERSITY OF COPENHAGEN PhD 2013; MSc 2008; BSc 2006

Dr Aishwarya G. Nadadhur (
Astrocytes are the most abundant glial cells in the central nervous system, which support and enable proper functioning of neurons. Recently there is evidence that astrocytes loose neurosupportive features in dementia related disorders. I am interested in understanding the role of astrocytes in tauopathies like Frontotemporal dementia (FTD) and Alzheimer’s disease (AD) using human iPSCs and mouse models. Specifically, I use patient iPSCs and gene corrected iPSC lines to generate neurons and astrocytes and study the neurosupportive roles of patient iPSC-derived astrocytes. My goal in this study is to identify important neurosupportive factors secreted by astrocytes that are altered in the tau related neurodegeneration. 

  • Alzheimer's Society Funded Researcher

Dr Katrina Räty (Albert) (
I am interested in modelling alpha-synuclein-based neurodegeneration in Parkinson’s disease. How is alpha-synuclein aggregating in Parkinson's and how it may be involved in toxicity of dopamine neurons in patients are central questions of my research. I have previously used toxin models of Parkinson’s disease as well as alpha-synuclein overexpression models extensively. I am currently working with a genetic model of alpha-synuclein developed in the lab to further understand the disease mechanisms.

  • Clare Hall Research Fellowship
  • University of Helsinki PhD 2019; MSc 2013; Carleton University BSc 2011



Dr Aviva Tolkovsky (
Nerve cells are complicated highly branched cells that are essential for our brains and our bodies. Without nerve cells we cannot think, feel, walk, pump blood or digest our food. The protein tau is a nerve cell protein that enables neurons to distribute essential proteins to distant parts of the cell in the brain, spinal cord, and in neurons that mediate sensation and control the actions of our internal organs. In Alzheimer's disease, tau ceases to function normally; it becomes misfolded and eventually forms neurofibrillary tangles (NFT) that are thought to be critical for neurodegeneration in the disease.Quite a lot is known about pathological changes that occur in tau, but one fundamental problem is still unanswered: what form of tau is truly pathological and how tau causes the nerve cells to die? These problems are difficult to solve by looking at the nervous system in post-mortem human brains because it is difficult to catch a dying nerve cell as dead nerve cells are rapidly cleared by neighbouring cells. For this reason, mouse models of tauopathy have been created where several features of the disease are replicated. However, even in mice, the dying cells in the brain are not easily accessible. To reduce animal use and still be able to investigate how tau kills cells, we have turned to a cell culture system of nerve cells from the sensory nervous system. We now know that cell death is not necessarily a random process. It can involve the orderly demolition of the cell. We develop models to determine the pathways by which tau causes nerve cell pathology and death. We also wish to explore whether we can keep the sick nerve cells alive using drugs that are being developed for eventual use in humans.
  • Associate Editor of journal AutophagyMember of the Secretariat of the International Cell Death Society (ICDS); Referee for Nature, Nature Medicine, Journal of Neuroscience and other major journals and of major grant funding bodies in the UK, Europe, USA, and Australasia
  • Former panel member of the Showcase Innovation grants review committee, The Wellcome Trust
  • HEBREW UNIVERSITY of JERUSALEM PhD 1975; MSc 1973; BSc 1972

​Image: Brain sections from two transgenic littermates expressing mutated tau protein stained with Cresyl Violet. Left panel shows healthy neurons in a mouse before disease onset, right hand panel shows swollen balloon neurons close to death from a symptomatic mouse


PhD Students



Janine Brandes (
Parkinson’s disease is characterised by progressive loss of neurons in specific areas of the brain, causing a range of motor and non-motor symptoms. This loss is preceded by neuronal dysfunction, possibly caused by intracellular aggregation of a protein called alpha-synuclein and sustained neuroinflammation. I am interested in better understanding this process, specifically how alpha-synuclein pathology and microglia alter neuronal communication and metabolism throughout the progression of the disease. For that purpose, I am working on establishing a cellular model of the human midbrain, the region most affected in Parkinson’s. I use induced pluripotent stem cells (iPSCs) derived from Parkinson’s patients, as well as their isogenic and healthy controls to generate midbrain-like organoids and microglia-like cells. When put together in a co-culture, those cells create a powerful tool to study the processes underlying cellular dysfunction in Parkinson’s.

  • Gates Cambridge Scholar
  • UNIVERSITY OF TUBINGEN Master of Science 2019; Bachelor of Science 2016



Joana Domingues (
Parkinson's disease is usually thought of as a movement disorder of the brain. As the disease progesses, we can observe the protein alpha-synuclein aggregating and these aggregates spreading through the brian. However, we do not know why the aggregation begins or the source of the initial aggregated alpha-synuclein.
The aim of my PhD project is to characterise a new transgenic mouse model that expresses the protein alpha-synuclein specifically in the gut. This will help us test the emerging hypothesis that alpha-synuclein aggregates can spread from the gut to the brain, via the nerves that control the gut. If this hypothesis is correct, we will be able to test treatments that could stop alpha-synuclein aggregates spreading to the brain, leading to the development of Parkinson's disease.
  • Member of Gonville and Caius College
  • Fellow of Marie Sklodowska-Curie ITN SynDegen

Image: Cross-section of mouse's small intestine showing neuronal cells (green) and Glial cells (red)

Matthew Mason (
Ageing is one of the greatest risk factors for idiopathic neurodegenerative disease. Indeed, in recent years, it has been demonstrated that there is a significant degree of overlap between the cellular changes that occur in natural ageing and those that occur in neurodegenerative disease. The objective of my PhD project is to investigate this overlap, with a specific focus on the activity of glia in these contexts. To this end, I am generating cortical organoids and iPSC-derived microglia, to explore in vitro how disease-relevant stimuli and ageing-relevant stimuli might dovetail to perturb the function of microglia.
  • Member of Gonville and Caius College 
  • BBSRC CASE Industrial Studentship, in collaboration with Eli Lilly & Company 
  • UNIVERSITY OF SOUTHAMPTON MSc (Integrated) 1:1 2018


Research Assistant



Helen Henson  (
I work in a collaborative project between the Department of Clinical Neurosciences and Department of Chemistry to directly image protein aggregates, tau and α-synuclein in iPSC-derived neurones and their lysate using super-resolution imaging, to determine how and why aggregates accumulate over time, their degradation and to map the number, composition, structure and size of the aggregates, which leads to neuronal death and thus the development of neurodegenerative diseases such as Alzheimer’s Disease, Parkinson’s Disease and Frontotemporal dementia (FTD-17P).

  • KEELE UNIVERSITY (Institute for Science & Technology in Medicine) MSc 2017; BSc 1:1 (hons) 2016