Per Lindqvist

First, I would like to thank the Grönberg Foundation for the support we in Umeå have received for our research on cardiac amyloidosis, we are very proud and happy for this support!

Our research draws heavily on our long-standing knowledge of systemic amyloidosis due to hereditary transthyretin-induced amyloidosis, or 'spoon disease' as it is commonly known.
With this knowledge, we now also have a good picture of the prevalence of the non-hereditary variant, known as wild-type or senile systemic cardiac amyloidosis. This type is often missed among elderly heart failure patients and is probably also the most common type. Amyloidosis has been successfully investigated both clinically and cell biologically/biochemically by researchers in Umeå. Such a constellation of bench-to-bedside research is a brilliant model for academic and clinical research. Systemic amyloidosis negatively affects many of the body's organs and one of these is the heart. The heart is deposited by transthyretin which makes the heart stiff and limited in its function.
Knowledge about amyloidosis is becoming even more relevant as new treatment methods are now available and new ones are also underway, such as the gene scissors (CRISPR-Cas9). With this knowledge, we in Umeå have developed an investigation plan that significantly shortens the time to correct diagnosis of cardiac amyloidosis. Together, this has given Umeå a leading position in Sweden and also internationally in these investigations and we are today awarded to be one of three with permission to conduct highly specialized care for systemic amyloidosis.

Once again, many thanks for this important support