Neurodegenerative Dementias (NDs) are progressive and irreversible due to brain cells’ deterioration and their interconnections. It is commonly believed that a loss of one or more protein homeostasis is observed in each of the NDs: Alzheimer’s dementia (AD: amyloid-β, tau), Lewy body dementia (LBD: α-synuclein, amyloid-β), and frontotemporal lobar dementia (FTD: tau, TDP43, FUS). Among the routinely used ND diagnostic methods today, brain imaging techniques pose cost-related hurdles, and collection of cerebrospinal fluid (CSF) is invasive.

Conversely, blood tests provide a viable alternative that is cost effective, widely available and non-invasive. In this context, works have shown that biomarkers like amyloid-β, TDP-43 and P-tau in plasma correlate with AD etiology and its progression.

However, beyond simple AD diagnostic considerations, the use of blood biomarkers seems inadequate due to the complex topographic, subcellular and temporal mosaic of proteins aggregation observed in NDs.

Since 2019, the Richetin Lab has developed numerous translational research approaches and works in close collaboration with the Memory Center (CLM-CHUV) and the Elderly Psychiatry Service (SUPAA-CHUV). Our priority is to stay as close as possible to the issues that are important to the patient and the clinical teams that treat them.

Our missions are :

1) Understand links between tau dysregulation and cognitive disorders during aging

2) Develop new methods for early diagnosis and stratification of dementia

3) Develop new approaches to restore brain homeostasis during pathological aging