MRI scan may offer faster way to detect Alzheimer's
Measuring specific changes in the brain using an MRI scan may help doctors diagnose Alzheimer's disease much earlier than standard diagnostic tests, new Canadian research says.
Researchers at the University of Western Ontario looked at the use of magnetic resonance imaging scans to monitor the expansion of fluid-filled cavities -- or ventricles -- in the brain, and the death of surrounding brain tissue.
The disintegration of brain tissue is linked to the cognitive impairment that is a hallmark of Alzheimer's.
"Right now, the diagnosis of Alzheimer's comes when a lot of brain tissue has been lost," study author Dr. Robert Bartha told CTV News.
"If we can diagnose it early, we can treat it."
Alzheimer's is currently diagnosed via a series of cognitive tests, such as memory and problem-solving assessments.
The research was led by Bartha of the Robarts Research Institute at Western. The findings are published in the online edition of the journal Brain.
The scientists studied MRI scans of 500 people over the age of 70 who either had no cognitive impairment, some cognitive impairment or who had been diagnosed with Alzheimer's.
They found that in healthy seniors, ventricles grow at a rate of about 1.5 per cent over six months as brain tissue shrinks during the normal aging process.
However, in seniors who exhibit early signs of cognitive difficulties, ventricles grow at a rate of about 3.5 per cent over six months.
And in seniors with Alzheimer's disease, ventricles grow at a rate of 5.5 per cent per six months.
Therefore, MRI scans will be a more definitive way to diagnose Alzheimer's.
"This allows us to find the disease earlier, because we are now looking at changes in brain tissue, rather than looking at consequences on memory and behaviour," Dr. Michael Borrie of the Lawson Health Research Institute in London, Ont., told CTV News.
The findings also suggest that doctors will be able to use the scans to assess if new drug treatments are effectively slowing damage to the brain.
Based on a report by CTV medical specialist Avis Favaro and senior producer Elizabeth St. Philip
Ventricular enlargement as a possible measure of Alzheimer's disease progression validated using the Alzheimer's disease neuroimaging initiative database
Sean M. Nestor, Raul Rupsingh, Michael Borrie, Matthew Smith, Vittorio Accomazzi, Jennie L.Wells, Jennifer Fogarty, Robert Bartha
Ventricular enlargement may be an objective and sensitive measure of neuropathological change associated with mild cognitive impairment (MCI) and Alzheimer's disease (AD), suitable to assess disease progression for multi-centre studies. This study compared (i) ventricular enlargement after six months in subjects with MCI, AD and normal elderly controls (NEC) in a multi-centre study, (ii) volumetric and cognitive changes between Apolipoprotein E genotypes, (iii) ventricular enlargement in subjects who progressed from MCI to AD, and (iv) sample sizes for multi-centre MCI and AD studies based on measures of ventricular enlargement. Three dimensional T1-weighted MRI and cognitive measures were acquired from 504 subjects (NEC n=152, MCI n=247 and AD n= 105) participating in the multi-centre Alzheimer's Disease Neuroimaging Initiative. Cerebral ventricular volume was quantified at baseline and after six months using semi-automated software. For the primary analysis of ventricle and neurocognitive measures, between group differences were evaluated using an analysis of covariance, and repeated measures t-tests were used for within group comparisons. For secondary analyses, all groups were dichotomized for Apolipoprotein E genotype based on the presence of an e4 polymorphism. In addition, the MCI group was dichotomized into those individuals who progressed to a clinical diagnosis of AD, and those subjects that remained stable with MCI after six months. Group differences on neurocognitive and ventricle measures were evaluated by independent t-tests. General sample size calculations were computed for all groups derived from ventricle measurements and neurocognitive scores. The AD group had greater ventricular enlargement compared to both subjects with MCI (P=0.0004) and NEC (P_0.0001), and subjects with MCI had a greater rate of ventricular enlargement compared to NEC (P= 0.0001). MCI subjects that progressed to clinical AD after six months had greater ventricular enlargement than stable MCI subjects (P= 0.0270).Ventricular enlargement was different between Apolipoprotein E genotypes within the AD group (P= 0.010).The number of subjects required to demonstrate a 20% change in ventricular enlargement was substantially lower than that required to demonstrate a 20% change in cognitive scores. Ventricular enlargement represents a feasible short-term marker of disease progression in subjects with MCI and subjects with AD for multi-centre studies.