Scientists have found that eliminating an enzyme from mice with symptoms of Alzheimer’s disease leads to a 90 percent reduction in the compounds responsible for formation of the plaques linked to this form of dementia — the most dramatic reduction in this compound reported to date in published research.

After a summer marred by disappointing clinical-trial results in patients with Alzheimer’s disease, drug developers are regrouping to plot a fresh course in the battle against the devastating disorder.

The bad news began in July and August, when Johnson & Johnson and Pfizer learned that their biological drug bapineuzumab had failed to show any benefit in two large trials. Then, on 24 August, Eli Lilly said that its drug solanezumab had not hit its goal of significantly slowing the memory decline and dementia that characterize Alzheimer’s disease.

Both of the failed drugs targeted amyloid-β, a protein that forms plaques in the brains of patients with the disease and that has long been the prime suspect for causing it. But rather than abandoning the amyloid hypothesis, scientists are pinning their hopes on innovative clinical-trial designs and new diagnostics that would allow them to test compounds earlier in the disease and gauge their efficacy more quickly.

Women with Alzheimer’s show worse mental deterioration than men with the disease, even when at the same stage of the condition, according to researchers from the University of Hertfordshire.

In the paper published in the Journal of Clinical and Experimental Neuropsychology, the researchers discovered that men with Alzheimer’s consistently and significantly performed better than women with the disease across the five cognitive areas they examined. Most remarkably, the verbal skills of women with Alzheimer’s are worse when compared to men with the disease, which is a striking difference to the profile for the healthy population where females have a distinct advantage.

Goldilocks was on to something when she preferred everything “just right.” Harvard Medical School researchers have found that when it comes to the length of mitochondria, the power-producing organelles, applying the fairy tale’s mantra is crucial to the health of a cell. More specifically, abnormalities in mitochondrial length promote the development of neurodegenerative diseases such as Alzheimer’s.

"There had been a fair amount of interest in mitochondria in Alzheimer’s and tau-related diseases, but causality was unknown," said Brian DuBoff, first author of the study and a post-doctoral research fellow at Massachusetts General Hospital.

"Ultimately, a deeper understanding of the relationship between mitochondrial function and Alzheimer’s may guide us to develop more targeted therapies in the future," said Mel Feany, HMS professor of pathology at Brigham and Women’s Hospital and senior author of the paper.

The findings were published online in the August 23 issue of Neuron.

Blood Test for Alzheimer’s Gaining Ground

Hu and his collaborators at the University of Pennsylvania and Washington University, St. Louis, measured the levels of 190 proteins in the blood of 600 study participants at those institutions. Study participants included healthy volunteers and those who had been diagnosed with Alzheimer’s disease or mild cognitive impairment (MCI). MCI, often considered a harbinger for Alzheimer’s disease, causes a slight but measurable decline in cognitive abilities.

A subset of the 190 protein levels (17) were significantly different in people with MCI or Alzheimer’s. When those markers were checked against data from 566 people participating in the multicenter Alzheimer’s Disease Neuroimaging Initiative, only four markers remained: apolipoprotein E, B-type natriuretic peptide, C-reactive protein and pancreatic polypeptide.

Changes in levels of these four proteins in blood also correlated with measurements from the same patients of the levels of proteins [beta-amyloid] in cerebrospinal fluid that previously have been connected with Alzheimer’s. The analysis grouped together people with MCI, who are at high risk of developing Alzheimer’s, and full Alzheimer’s.

“We were looking for a sensitive signal,” says Hu. “MCI has been hypothesized to be an early phase of AD, and sensitive markers that capture the physiological changes in both MCI and AD would be most helpful clinically.”

Artificial Butter Flavoring Ingredient Linked to Key Alzheimer’s Disease Process

A new study raises concern about chronic exposure of workers in industry to a food flavoring ingredient used to produce the distinctive buttery flavor and aroma of microwave popcorn, margarines, snack foods, candy, baked goods, pet foods and other products. It found evidence that the ingredient, diacetyl (DA), intensifies the damaging effects of an abnormal brain protein linked to Alzheimer’s disease. The study appears in ACS’ journal Chemical Research in Toxicology.

Alzheimer’s villain cures multiple sclerosis in mice

A notorious biochemical villain has just revealed its heroic side. Beta-amyloid, a misfolded protein fragment blamed for killing brain cells in Alzheimer’s disease, has reversed the symptoms of mice suffering from the rodent equivalent of multiple sclerosis (MS).

MS occurs when the immune system mistakenly attacks the fatty myelin sheaths around nerve fibres that serve as electrical insulation. Without this insulation, nervous impulses falter, leading to physical and cognitive problems. Myelin increases the speed at which electrical impulses travel around the body.

As it is destroyed, nerve communication falters, leading to physical and cognitive problems. Lawrence Steinman of Stanford University in California had expected amyloid-beta to exacerbate this damage, given that it is toxic to neurons and builds up where myelin sheaths are being destroyed.

How the Brain and Nerve Cells Change During Alzheimer’s Disease

One of the hallmarks of Alzheimer’s disease is the accumulation of amyloid plaques between nerve cells (neurons) in the brain. Beta amyloid is a fragment of a protein snipped from another protein called amyloid precursor protein (APP). In a healthy brain, these protein fragments would break down and be eliminated. In Alzheimer’s disease, the fragments accumulate to form hard, insoluble plaques.

Neurofibrillary tangles are insoluble twisted fibers found inside the brain’s nerve cells. They primarily consist of a protein called tau, which forms part of a structure called a microtubule. The microtubule helps transport nutrients and other important substances from one part of the nerve cell to another. Axons are long threadlike extensions that conduct nerve impulses away from the nerve cell; dendrites are short branched threadlike extensions that conduct nerve impulses towards the nerve cell body. In Alzheimer’s disease the tau protein is abnormal and the microtubule structures collapse.

As Alzheimer’s disease spreads through the cerebral cortex (the outer layer of the brain), judgment worsens, emotional outbursts may occur and language is impaired. Memory worsens and may become almost non-existent. On average, those with Alzheimer’s live for 8 to 10 years after diagnosis, but this terminal disease can last for as long as 20 years.