Dementia research is expanding its horizons beyond the traditional focus on brain proteins. For over a century, the amyloid hypothesis has been a primary framework for understanding Alzheimer’s disease. This theory stems from the discovery of amyloid plaques by Alois Alzheimer in 1906. While these protein clumps, along with tau tangles, are key characteristics of Alzheimer’s, not everyone with these proteins develops dementia. This revelation has spurred interest in exploring other potential contributors like diabetes and herpes, which may play significant roles in dementia’s onset.
Dementia research is increasingly investigating links to conditions like diabetes and herpes. Historically dominated by the amyloid hypothesis, which connects amyloid plaques and tau tangles to Alzheimer’s, studies reveal that these plaques do not always lead to dementia symptoms. This statement encourages a wider examination of possible causes contributing to dementia.
The exploration of dementia is moving towards understanding multiple factors beyond amyloid and tau proteins, suggesting diabetes and herpes may influence the disease’s development. This shift recognises that not all individuals with amyloid deposits exhibit dementia symptoms, inviting a fresh perspective on the condition’s complexities and a broader pathway for research.
Original Source: www.scmp.com
