Inflammation in the brain is usually seen as harmful in the aging process—it’s thought to contribute to Alzheimer’s and dementia. But a new study in mice suggests that inflammation, led by an immune molecule called STING, might have a role in protecting the aging brain. The findings also have implications for new experimental Alzheimer’s drugs that are designed to block STING.

A new analysis of 15 years of clinical and genomic data from the UK BioBank and 2 other public resources has found that people who had been diagnosed with select gut diseases – such as functional intestinal disorders – also had a higher likelihood of developing Alzheimer’s disease (AD) and Parkinson’s disease (PD). By harnessing these massive databases, the work explores the relationship between gut disruptions and neurodegeneration, incorporating genetics and proteomics in its characterizations. Conditions in the gut can influence brain health and vice versa. Teasing out the intricacies of this connection – especially the relationship between neurodegenerative diseases, such as AD and PD, and digestive disorders – could help scientists identify disease predictors and improve techniques for early detection and treatment. Using data from the UK Biobank, the SAIL databank, and the FinnGen project, Mohammad Shafieinouri and colleagues investigated correlations between 155 diagnoses for nutritional, metabolic, digestive, and endocrine disorders. They used statistical models that examined the connection between the time of diagnosis for gut-brain disorders and the time of AD or PD diagnosis (spanning 1 to 5, 5 to 10, and 10 to 15 years prior to AD or PD). The clinical data featured more than 502,000 people. They also employed linear models from UK BioBank data to generate polygenic risk scores and assess 1,463 known proteomic biomarkers. The genetic data included more than 487,000 people, and the proteomic data included more than 52,000 people. Overall, Shafieinouri et al. found that any co-occurring gut diagnosis contributes to AD or PD risk, corroborating existing work. There was no statistically significant correlation between years between diagnosis and neurodegeneration onset. Within these gut diagnoses, people with non-infective colitis, gastritis, and oesophagitis had a higher rate of developing AD or PD. This relationship also appeared with functional intestinal disorders. The team also developed an interactive resource to see the breakdown between comorbidities and likelihood of AD or PD.

One of the great challenges faced by families coping with Alzheimer’s disease and other forms of dementia is learning how to communicate effectively with the person impacted by the disease while also upholding their personhood, or sense of personal value. A new study from UConn researcher Amanda Cooper – published in time for World Alzheimer’s Month in September and World Alzheimer’s Day on Sept. 21 - offers concrete recommendations on what to do and what not to do to support personhood for a family member living with dementia. This study, “Finding the Communication Sweet Spot: Strategies Promoting Personhood in Conversations Between Individuals with Dementia and Their Family Members,” was published in the Journal of Family Communication in July.

A molecular mechanism that significantly contributes to the progression of Alzheimer’s disease has been discovered by a research team led by neurobiologist Prof. Dr Hilmar Bading of Heidelberg University. In joint experiments with researchers from Shandong University (China), the team, using an Alzheimer’s mouse model, demonstrated that a neurotoxic protein-protein complex is responsible for nerve cells in the brain dying off and the resulting cognitive decline. According to the scientists, this finding opens up new perspectives for the development of effective treatments.