Rethinking the cause of Alzheimer's disease

The accepted view as to what causes Alzheimer’s disease has been questioned by a new QUT study.

Previously it was thought that a build-up of amyloid proteins in the brain was a trigger for Alzheimer’s; however, researchers have said that a paradigm shift in thinking may be needed.

PhD candidate Martina Gyimesi, Dr Rachel Okolicsanyi and Associate Professor Larisa Haupt, from the QUT School of Biomedical Sciences, said that tau protein ‘tangles’ in the brain were symptoms, rather than the initiators, of the most common form of dementia.

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,” she 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.”

Haupt said recent studies had proposed 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,” she 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.”

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