Scientists at the University of Pennsylvania have developed a screening test for Alzheimer’s disease.

They claim the test can detect the condition before symptom onset and predict whether patients with mild cognitive impairment will progress to the full-blown syndrome.
 
The test involves measuring cerebrospinal fluid concentrations of the disease’s 2 principal biochemical hallmarks—amyloid beta42 peptide and tau protein.

Compared with unaffected people, Alzheimer’s patients have decreased levels of the former and increased levels of the latter.
 
“With this test, we can detect and track progression of Alzheimer’s disease,” Leslie Shaw asserted to BurrillReport.

The co-director of Penn’s Alzheimer’s Disease Neuroimaging Initiative and lead author of the study added, “validated biomarkers will improve the focus of Alzheimer’s clinical trials, enrolling patients at earlier stages of the disease to find treatments that can delay, and perhaps stop neurodegeneration.”
 
Shaw and her colleagues wrote it up in Annals of Neurology.

The scientists examined CSF samples from 410 volunteers at 56 sites in the US and Canada, as well as 52 presumed normal volunteers and post-mortem specimens from 56 patients with autopsy-proven Alzheimer’s disease.
 
The test was 87 percent accurate overall.

It correctly ruled out Alzheimer’s in 95% of normal volunteers, correctly detected the disease in 96% of those with autopsy-proven disease, and predicted conversion from mild cognitive impairment to Alzheimer’s in 82% of participants.

Further validation studies are underway. 
 
“We have validated a test where a safe, simple lumbar puncture can provide information to confirm suspected Alzheimer’s disease and predict the onset of the disease,” John Trojanowski told Burrill.

The director of the Penn Alzheimer’s Disease Core Center added that “using this technique, we will further our understanding of how the disease progresses and what we can do to stop Alzheimer’s disease before it starts.”

Diabetes and strokes precipitate age-related cognitive decline by impacting the hippocampus, a part of the brain involved in memory formation.

But the 2 conditions affect different parts of the hippocampus and do so via different mechanisms, according to a study in Annals of Neurology.

Scott Small and colleagues at Columbia University Medical Center used magnetic resonance imaging to document strokes and create functional maps of the hippocampus in 240 community-based elderly individuals including 60 with diabetes and 74 with brain infarcts.

They found that diabetes impacted hippocampal function via swings in blood glucose levels, while strokes impacted a different subregion via transient reductions in blood flow.

In the case of diabetes, adverse effects on the brain were correlated with mild to moderate blood sugar excursions, a conclusion that may have implications for so-called “normal, age-related” cognitive decline, because glucose regulation starts to deteriorate by the fourth decade of life.

“If we conclude this is underlying normal age-related cognitive decline, then it affects all of us,” Small told the New York Times.

And since physical exercise improves glucose regulation, “We have a behavioral recommendation — physical exercise,” he added.

Bruce S. McEwen, a neuroendocrinologist at Rockefeller University was impressed. “When we think about diabetes, we think about heart disease and all the consequences for the rest of the body, but we usually don’t think about the brain,” he said.

“We need to think about their…cognitive skills, and whether they will be able to keep up with the demands of education and a fast-paced society.”

Earlier studies had demonstrated that physical activity reduces the risk and diabetes increases the risk of age-related cognitive decline.