Scientists have identified a unique odour signature in urine which could help develop a non-invasive tool for early diagnosis of Alzheimer’s disease.
The odour signature found in mouse models of the disease appears in urine before significant development of Alzheimer-related brain pathology, researchers said.
Identification of an early biomarker for Alzheimer’s disease could potentially allow physicians to diagnose the debilitating disorder before the onset of brain decline and mental deterioration, paving the way for upcoming treatments to slow early progression of the disease.
“Now we have evidence that urinary odour signatures can be altered by changes in the brain characteristic of Alzheimer’s disease,” said Bruce Kimball, from the US Department of Agriculture’s (USDA) National Wildlife Research Centre (NWRC) who is stationed at the Monell Centre.
Alzheimer’s is the most common form of dementia. There is no test to definitively diagnose Alzheimer’s disease.
Although the progression of Alzheimer’s currently cannot be stopped or reversed, an accurate diagnosis can give patients and families time to plan for the future and seek treatments for symptom relief.
In the study, researchers studied three separate mouse models, known as APP mice, which mimic Alzheimer’s-related brain pathology.
Using both behavioural and chemical analyses, the researchers found that each strain of APP mice produced urinary odour profiles that could be distinguished from those of control mice.
The odour differences between APP and control mice were mostly independent of age and preceded detectable amounts of plaque build-up in the brains of the APP mice.
These findings suggest that the characteristic odour signature is related to the presence of an underlying gene rather than to the actual development of pathological changes in the brain.
Additional studies showed that the distinctive odour profiles could be used to predicatively identify APP mice versus control mice.
One of the hallmark pathological indicators of Alzheimer’s disease is an excess formation of amyloid plaque deposits in the brain, researchers said.
Scientists mimic this pathology in mouse models by introducing human genes associated with mutations of the amyloid-beta precursor protein gene into the mouse genome.
These genes are then pharmacologically activated to make excess amyloid-beta protein, leading to plaque buildup in the brains of APP mice.