Alzheimer's disease: scientific dissemination actions for non-specialized audiences

• Grant number: 24/00610-8
• Support Opportunities: Scholarships in Brazil - Scientific Journalism
• Start date: May 01, 2024
• End date: April 30, 2025
• Field of knowledge: Biological Sciences - Morphology - Cytology and Cell Biology
• Principal Investigator: Marimélia Aparecida Porcionatto
• Grantee: Alex Mota Cavalcante
• Host Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil
• Associated research grant: 18/12605-8 - Development of brain-on-a-chip microplataforms for in vitro modeling of the central nervous system, AP.TEM

Abstract

The increase in life expectancy in recent decades, while reflecting positive public health measures, poses new challenges due to the increased incidence of chronic non-communicable diseases. Diabetes, cardiovascular diseases, and neurodegenerative diseases, including Alzheimer's disease (AD), are among the main diseases that affect the health of the world's population today. AD can be classified as familial (fAD, familial Alzheimer's disease) or sporadic (sAD, sporadic Alzheimer's disease), this form being the most prevalent, accounting for 90-95% of cases. The number of people diagnosed with AD has increased by almost 150% in the last 20 years, and the prediction is that in 2030, around 80 million people in the world will have AD, reaching more than 130 million in 2050. Early diagnosis and treatment are still two major challenges to be overcome. fAD and sAD present similar symptoms and cellular and molecular markers. Among these markers are the accumulation of beta-amyloid oligomers in the brain extracellular matrix and neurofibrillary tangles caused by hyperphosphorylation of the Tau protein within neurons. fAD is caused by mutations in the APP, PSEN1, and PSEN2 genes, while the cellular and molecular mechanisms for sAD are not yet fully understood. Several risk factors for sAD have already been identified, including age, sex, obesity, and diabetes. However, none alone determines the disease, making understanding the pathophysiology of the sporadic form more complex. Studies also point to the association of APOE genotypes with the development of sAD, with the APOE4 allele considered a risk factor, while the APOE2 allele is considered a protective factor. Animal models, especially transgenic mice, have been the primary model for fAD studies, and models for sAD are still scarce. Recently, cortical organoids and chips have started to be used to model, mainly, fAD. Our group has been working on developing three-dimensional (3D) in vitro models for sAD, focusing on reproducing the microenvironment of type 2 diabetes, with exposure of neurons, astrocytes, and endothelial cells to high glucose and advanced glycation products. The number of scientific works referring to AD indexed in PubMed has almost quintuplicated in the last 20 years, reflecting the growing concern of the scientific community. The large volume of research results in AD, especially in the search for early biomarkers and new treatments, is almost inaccessible to the non-specialized public. It is necessary to translate scientific language into understandable terms to clarify the public, including patients, families, and people involved in caring for patients with AD. Using different communication tools, such as podcast production, videos, and posts on social networks, we intend to contribute to the dissemination of scientific knowledge generated from research in AD, developed in our group and available in scientific literature, resulting in a better understanding of the different aspects of AD, enabling decision-making based on scientific knowledge.