Recipient organisationNIHR Southampton Biomedical Research Centre
NIHR supportRecorded as supported by this research centre
PeriodMar 2025 — Mar 2026
In plain English
AI plain-English summary
Doctors struggle to tell different types of dementia apart, especially early on, because the symptoms overlap so much. This project will analyse cerebrospinal fluid from patients for markers of inflammation and blood vessel damage, then link those findings to brain scans and symptom scores. The problem is that current diagnostic tools—brain imaging and fluid biomarkers—cannot reliably predict how fast a patient’s cognitive decline will progress. Recent evidence suggests that immune system activation and inflammatory mediators can worsen Alzheimer’s disease by driving abnormal protein production and neuron loss. But it remains unclear whether specific immune signatures, rather than single biomarkers, are linked to different dementia subtypes or faster progression. If this pilot study succeeds, it could identify novel immune pathways that connect inflammation in the cerebrospinal fluid to clinically defined dementia and its progression. That would open the door to more accurate diagnosis and, potentially, future therapies that modulate those immune pathways to slow or prevent Alzheimer’s disease. Better diagnostic precision would directly improve patient care by matching people to the right treatments and support earlier.
View original technical description
Many neurological diseases present with similar cognitive, behavioural and/or movement symptoms, particularly in the early stages of disease. This hampers accurate diagnosis of dementia, and patient care could be substantially improved with more accurate identification of type of dementia and prediction of future decline.Clinicians have access to an increasing array of tools to assist in the diagnosis of dementia, including brain imaging techniques and fluid biomarkers such as cerebrospinal fluid (CSF). Despite these new developments in diagnosis, the available fluid and imaging biomarkers do not yet accurately predict the rate of cognitive decline, suggesting that additional factors may influence disease severity and/or progression. Recent studies have shown convincing evidence that activation of the immune system can influence Alzheimer’s disease progression and/or severity. This is mediated by inflammatory mediators, which exacerbate the production of abnormal proteins and neuronal loss. Evaluating inflammatory biomarkers in the CSF and/or blood may therefore provide enhanced diagnostic results. An important outstanding question is whether specific immune pathways, or signatures, rather than individual biomarkers, can be identified in the CSF and linked with increased risk of disease progression, or dementia subtypes. Modulation of these immune pathways could lead to future therapeutic or preventive strategies for Alzheimer's.In this project, we aim to study the link between neuroinflammation and brain function in patients with dementia. In this proposal, we will analyse CSF samples for the presence of inflammation and vascular injury markers. These novel CSF biomarker findings will be linked to patient functional levels and symptom inventory scores, and brain patterns on imaging. Our proposed study will generate pilot data towards the identification of novel immune pathways that link inflammation in CSF to clinically defined dementia and its progression.
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