Spinal fluid testing, combined with MRI scans could provide early warning signs of a developing Alzheimer's condition. A team of researchers from the Institute, part-funded by the Alzheimer's Research Trust, has discovered and shared online in this week's edition of Annals of Neurology.

In 2006, there were 26.6 million sufferers worldwide. Alzheimer's is predicted to affect 1 in 85 people globally by 2050. This incurable, degenerative, and terminal disease was first described by German psychiatrist and neuropathologist Alois Alzheimer in 1906 and was named after him. Most often, it is diagnosed in people over 65 years of age, although the less-prevalent early-onset Alzheimer's can occur much earlier.

This new approach to symptom identification could allow scientists to test treatments or preventions far earlier in the disease, when they could be more effective.

Dr. Jonathan Schott from the Dementia Research Center at the UCL Institute of Neurology says: "In this study of healthy people in their 70s and 80s we found that about one in three had a spinal fluid profile consistent with Alzheimer's disease. Using MRI scanning, we showed that these individuals also had increased brain shrinkage over the following year." One hundred five cognitively normal persons from the Alzheimer's disease Neuroimaging Initiative (ADNI) were used in this new combination treatment study. They were divided into two groups: Those with high levels of cerebrospinal fluid amyloid (CSF), a protein which is typically reduced in the CSF of patients with Alzheimer's disease Those with opposite low levels of the protein. In addition, MRI scan measurements over a one year period were used to measure the brain shrinkage rate. The researchers at the Dementia Research Center also checked for the presence of known Alzheimer's risk gene APOE4. Apolipoprotein E (APOE) is a class of apolipoprotein found in the chylomicron and IDLs, that binds to a specific receptor on liver cells and peripheral cells. It is essential for the normal catabolism of triglyceride-rich lipoprotein constituents.

This comparison demonstrated that 38% of the group's CSF levels of amyloid shrank twice as rapidly as the other participants post MRI. In addition, this group was also five times more likely to possess the APOE4 risk gene and had higher levels of another culprit Alzheimer's protein, tau.

In a healthy person, tau protein interacts with a compound called tubulin to strengthen the neural tubes in the axons of neurons. The neural tubes essentially act like train tracks for signals to pass along the axon. Disruption in the level of tau protein can lead to instability in the neural tubes, which makes it difficult for neurons to pass signals along. This in turn can lead to neurological problems as the functioning of the central nervous system is interrupted, and depending on the area of the interruption, a patient can experience various symptoms.

Dr. Schott continues: "The significance of these findings will only be clear with longer clinical follow-up, but may suggest that these individuals are at increased risk of developing dementia. If so these results add to a growing body of work suggesting that Alzheimer's disease starts many years before the onset of symptoms." Rebecca Wood, Chief Executive of the Alzheimer's Research Trust, the leading UK dementia research charity reflects on the findings: "We are hamstrung by our inability to accurately detect Alzheimer's, but these findings could prove to be pivotal. Spotting Alzheimer's early is essential to the global research effort to beat the disease. We know that treatments for many diseases can be more successful if given early and this is likely to be true for Alzheimer's. It will be crucial to keep following the study group to see how many develop Alzheimer's, and to expand the research to test the approach further. Findings like these underline the importance of research, but detecting Alzheimer's is only the first step. If we are to defeat the disease, we must invest in research into preventions and treatments now before our dementia crisis spirals out of control." "Increased brain atrophy rates in cognitively normal older adults with low cerebrospinal fluid Aβ1-42"
Jonathan M. Schott MD, Jonathan W. Bartlett PhD, Nick C. Fox MD, Josephine Barnes PhD.
Annals of Neurology. DOI: 10.1002/ana.22315

Sy Kraft, B.A.