Skip to main content
Home » Dementia » Analysing the link between inflammation and dementia

Dr Magdalena Sastre

Reader in Molecular Neuroscience, Imperial College London

Currently, there is no cure for Alzheimer’s disease (AD). The efforts of the research community in the last decade have focused in targeting the cause of the disease (the presence of amyloid-β plaques and neurofibrillary tangles) but the results have not been encouraging, probably because the disease has spread already in those patients and is too late to stop. So, other avenues should be pursued or we should find ways to prevent or delay the progression of the disease.

My laboratory, and others at Imperial College London, are interested in the role of inflammation in Alzheimer’s disease (AD). It is known that processes leading to inflammation in the brain are a trigger for Alzheimer’s. For instance, patients with head injury are predisposed to suffer AD and their brains display amyloid plaques and neurofibrillary tangles.

In the Department of Brain Sciences, we are currently examining the brains from boxers as well as animal models of head injury to discover which mechanisms are involved, probably related to an increased inflammatory reaction in the brain. We can follow up these inflammatory changes by live imaging of the brains, using radioactive tracers that bind the inflammatory cells; Imperial has been pioneer in this technique.

The relationship between microbiomes and dementia

Not only does inflammation in the brain affect our chances of developing AD, but also the bacteria in our gut, which influences our immune system. At Imperial College, there are groups analysing the metabolic profile of gut bacterial communities to understand the relationship of certain microbiomes with dementia and brain health.

It is believed patients with diabetes have increased risk for AD due to vascular alterations and enhanced inflammation in their brains.

Gut microbiota has been implicated in metabolic diseases such as diabetes. It is believed patients with type 2 diabetes have increased risk for AD due to vascular alterations and enhanced inflammation in their brains. At Imperial we are studying these links using different approaches, including epidemiological studies on large prospective cohorts (conducted at the School of Public Health) and clinical trials with anti-diabetic drugs such as liraglutide.

Lastly, several groups at the Dementia Research Institute at Imperial are working on the effect of sleep deprivation, which might trigger or accelerate pathological processes leading to dementia, e.g. by causing oxidative stress or enhancing amyloid deposition.

Next article