A call to rethink the possible early cause of Alzheimer’s disease that challenges the accepted view of a build-up of amyloid proteins in the brain, has come from QUT scientists in an article in Open Biology.
- New approach questions cause of Alzheimer’s disease (AD) – toxic amyloid and tau proteins in brain
- Impaired production of new neurons in the hippocampus precedes amyloid and tau – therefore could initiate AD
- Study focussed on molecular pathways associated with neurogenesis in the brain’s memory formation region
PhD candidate Martina Gyimesi, Dr Rachel Okolicsanyi and Associate Professor Larisa Haupt, from the QUT School of Biomedical Sciences, suggest a paradigm shift in thinking is needed to explore the ‘triggers’ behind toxic amyloid and tau proteins.
The researchers said that these protein ‘tangles’ in the brain were symptoms, rather than the initiators of the most common form of dementia.
Ms Gyimesi said the current understanding of Alzheimer’s disease (AD) was that the onset of amyloid and tau protein build-up caused the brain deterioration seen in patients ultimately leading to death.
“We know that existing treatments targeting these hallmark pathologies offer only minimal relief of symptoms and do not significantly halt the progression of AD,” Ms Gyimesi said.
“Our review offers a broader, alternative view that centres on impaired adult hippocampal neurogenesis (AHN) as a potential early causal factor.
“AHN is the intricate process in which mature neurons are generated from human neural stem cells in the adult central nervous system.”
Professor Haupt said recent studies had suggested that AHN was diminished even before amyloid and tau proteins appeared, suggesting its initiating role in the early stages of AD development.
“We investigated molecular pathways regulating AHN, focusing on the specialised brain regions that are also responsible for memory formation,” Professor Haupt said.
“We identified disruptions and interactions within these pathways that may result in similar pathologies to pre-clinical AD.
“The key to treating AD may lie in understanding how and why the brain loses its ability to continue creating mature brain cells.
“This is an issue that is still relatively unexplored and by identifying potential molecular pathways for further investigation, we hope to shift the paradigm in AD research, encouraging scientists to look beyond amyloid and tau proteins in future studies.”
Beyond amyloid and tau: rethinking Alzheimer’s disease through less explored avenues was published in Open Biology.
(Image, from left: Dr Rachel Okolicsanyi, Martina Gyimesi, Associate Professor Larisa Haupt)