Vicky Jones

Dr. Vicky Jones

Senior Lecturer in Molecular Biology

School of Pharmacy and Biomedical Sciences

Maudland Building, MB024

+44 (0) 1772 89 5833

Subject Areas: Biological Sciences

Vicky joined UCLan as a lecturer in molecular biology in 2011. Her research focuses on unravelling the molecular mechanisms underlying neurodegenerative disorders such as Alzheimer’s disease.

Vicky is research active within the area of pharmacy and biomedical sciences and is a member of the Neuronal and Tissue Dysfunction Research Group.

Full Profile

After graduating from the University of Salford in 2003 with a BSc (Hons.) in Biochemistry, Vicky moved to the University of Manchester where she completed her PhD under the supervision of Prof. Alex Verkhratsky and Dr. Owen Jones. Her thesis, entitled “continuity in the neuronal endoplasmic reticulum”, focused on the development of two new lentivirally-delivered fluorescent reporters to visualise the endoplasmic reticulum (ER) in cultured neurons and in brain slices. Using these reporters Vicky provided the first direct evidence of a single, continuous ER lumen extending throughout the cell both in neurons and in astrocytes.

Vicky remained at the University of Manchester and undertook two postdoctoral research positions. The first built upon her PhD work, exploiting the newly developed fluorescent reporters to investigate the morphology and integrity ER in Alzheimer’s disease.

In her second postdoctoral position, Vicky joined the lab of Prof. Philip Woodman to investigate the role of accessory proteins in cargo sorting and intraluminal vesicle formation in the mammalian endocytic pathway.

Vicky took up her current position as lecturer in molecular biology at UCLan in 2011. Her research remains focussed on the cellular causes of neurodegenerative disorders, and Vicky is especially interested in the dysfunction of astrocytes associated with Alzheimer’s disease.

Vicky had an article published on The Conversation in March 2019 about research into the causes of Alzheimer’s disease entitled ‘Alzheimer’s disease: have we got the cause all wrong?

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Tyler AR, Okoh AO, Lawrence CL, Jones VC, Moffatt C, Smith RB (2013) N-Alkylated 2,3,3-trimethylindolenines and 2-methylbenzothiazoles. Potential lead compounds in the fight against Saccharomyces cerevisiae infections. Eur J Med Chem, 64C:222-227.

Jones VC, Rodríguez JJ, Verkhratsky A and Jones OT (2009) A lentivirally-delivered photoactivatable GFP to assess continuity in the endoplasmic reticulum of neurones and glia. Pflugers Archiv. 458(4):809-18.

Rodríguez JJ, Jones VC and Verkhratsky A (2009) Impaired cell proliferation in the subventricular zone in an Alzheimer’s disease model. Neuroreports, 10:907.

Rodríguez JJ, Jones VC, Tabuchi M, Allan SM, Knight EM, LaFerla FM, Oddo S, Verkhratsky A (2008) Impaired adult neurogenesis in the dentate gyrus of a triple transgenic mouse model of Alzheimer’s disease. PloS One, 3:e2935.

More publications


  • Ph.D. Neuroscience, University of Manchester, 2007
  • B.Sc. (Hons.) Biochemistry, University of Salford, 2003


Available projects include:

  • The development of a novel cell line model for Alzheimer's
  • The investigation of ER stress responses in dementia
  • The effect of Alzheimer's on the astrocytic endoplasmic reticulum
  • The effect of Alzheimer's on astrocytic apoptosis


Society for Experimental Biology.

Teaching Activities and Responsibilities


BSc Biomedical Science
BSc Biological Sciences
BSc Healthcare Science
BSc Physiology and Pharmacology
BSc Applied Biomolecular Sciences
BSc Neuroscience
MSc Cancer Biology and Therapy
MSc Biomedical Sciences
MSc Pharmaceutical Biotechnology


Year 1
BL1218: Scientific Basis of Healthcare
BL1220: Integrative Biological Sciences (Deputy Module Tutor)

Year 2
BL2203: Molecular and Cellular Biology (Module Tutor)
BL2215: Biostatistics (Module Tutor)
BL2216: Cellular Investigations

Year 3
BL3206: Biology of Disease

Year 4
BL4210: Cancer Biology
BL4214: Clinical Analysis
BL4215: Pharmaceutical Biotechnology
BL4224: Lab Based Research Techniques


Vicky’s research aims to uncover the subcellular mechanisms which govern the onset and progression of dementias, such as Alzheimer’s disease (AD). Specifically, Vicky is interested in exploring the calcium hypothesis of AD; the theory that disruption in intracellular calcium levels either triggers or worsens the brain cell death seen in this disease.

Much of the research conducted to date has focussed on calcium dysregulation in neurons, as it is these crucial impulse-carrying cells which die off in brain areas crucial for learning and memory. However, it is now known that neurons are not the only type of cell in the brain that is affected by AD, especially with regards to calcium homeostasis.

Part of the glial family of brain cells, astrocytes were long thought to be relatively quiescent cells; functioning only to nourish and support the neurons. In the last 20 years however their crucial role as subtle modulators of brain activity has emerged. For example, it has been shown that astrocytes envelop some synapses (junctions between neighbouring neurons) and can absorb or release chemicals which alter the transmission of information between the neurons.

Like other cells, calcium serves as an extremely important messenger in astrocytes. Through the action of the endoplasmic reticulum (ER; a large organelle extending throughout the cell), astrocytes can pass signals around the cell and even to neighbouring cells by carefully releasing stored calcium. This acts as an important communication mechanism that permits messages about brain activity in one region to be passed through a network of connected astrocytes to bring about changes in synapse function.

We now know that calcium handling in astrocytes is disturbed in Alzheimer’s disease, and we also know that this disturbance occurs long before any clinical symptoms of dementia are seen.

Vicky’s research is centred on finding out how Alzheimer’s affects astrocyte structure and function, and how this alteration in functioning may be implicated in the progression of the disease.

To this end, Vicky’s lab is currently investigating how mutant β-amyloid and presenilins (defective proteins associated with familial AD) affect the integrity of the astrocyte ER and the cell’s ability to protect against cell death. She is also working on the development of a new cell line of AD which can be grown easily in the lab to permit quick, inexpensive experiments.

Vicky Jones - Cells