by Richard Lenti for American News Report:

The use of pain medication may help decrease the anxiety, depression and loss of sleep often encountered by patients suffering from dementia, according to a new study.

British researchers followed 480 patients in specialized dementia care homes and found that with a 10% increase in a person’s pain medicine, there was a dramatic reduction in the use of anti-psychotic drugs and other medications.

The study was not peer-reviewed and was conducted by Four Seasons Health Care, which manages 56 dementia care centers in England.

“When people with dementia are showing distress reactions this may be due to them experiencing pain or discomfort, yet too often rather than trying to identify and relieve this symptom they are needlessly given anti-psychotic drugs to calm them and keep them quiet,” said Caroline Baker, head of quality and dementia care for Four Seasons Health Care.

“Reducing use of these drugs is a national priority. With a better understanding of how to care for people with dementia we can reduce the need for anti-psychotics together with a range of other medications and at the same time improve well-being.”

by Cynthia Billhartz Gregorian for Medical XPress:

Leslye Nathe did not realize the profound effect that Ritalin was having on her mother’s Alzheimer’s disease until a doctor stopped the prescription.

Her mother, Susan Brown, 74, a resident at Provision Living in Webster Groves, Mo., began sleeping nearly all the time. And during rare moments, when she was awake, she was tearing the sheets off of her bed and scratching wounds into her arms.

“She was like a child having a tantrum and she kept telling people to leave. She was very paranoid,” Nathe said. “She would beg me, ‘Please, please get me some medication. There’s something wrong. I can’t deal with it anymore.’” Brown had been taking Ritalin for many years even before she was diagnosed with Alzheimer’s, to treat attention deficit disorder and depression.

When her physician, Dr. George Grossberg, director of geriatric psychiatry at St. Louis University, heard about her alternating bouts of lethargy and meltdowns, he put Brown back on the Ritalin. Her reaction to being taken off the drug was more extreme than usual, but it supported the long-held notion that Ritalin is key to controlling some Alzheimer’s symptoms.

by Science Daily:

A team of researchers from Université Laval, CHU de Québec, and pharmaceutical firm GlaxoSmithKline (GSK) has discovered a way to stimulate the brain’s natural defense mechanisms in people with Alzheimer’s disease. This major breakthrough, details of which are presented January 15 in an early online edition of the Proceedings of the National Academy of Sciences (PNAS), opens the door to the development of a treatment for Alzheimer’s disease and a vaccine to prevent the illness.

One of the main characteristics of Alzheimer’s disease is the production in the brain of a toxic molecule known as amyloid beta. Microglial cells, the nervous system’s defenders, are unable to eliminate this substance, which forms deposits called senile plaques.

by John Gever for MedPage Today:

When drug giant Eli Lilly announced in August that both EXPEDITION trials of its anti-amyloid drug solanezumab had failed to show a significant benefit, many in the field thought that would be the end of the line for such agents, at least for patients showing clear signs of cognitive impairment.

The failure followed a string of other disappointing results with a variety of agents targeting the rogue protein.

Another monoclonal antibody drug, bapineuzumab, had also shown no clinical benefit in a large trial. Likewise, compounds aimed at inhibiting secretase enzymes responsible for producing beta-amyloid in vivo were disappointing.

And before that, an immunotherapy intended to mobilize the body’s own immune system against beta-amyloid plaques had also failed. Even staunch advocates of the so-called amyloid hypothesis in Alzheimer’s disease — which holds that beta-amyloid protein plaques are a key causative factor in the neurodegeneration that underlies the condition — had changed their thinking.

by Tess Stynes for 4-Traders:

Merck & Co. reached a collaboration, license and supply agreement with General Electric Co.’s health-care business for use of a GE Healthcare investigational imaging agent to support the pharmaceutical company’s lead drug candidate to treat Alzheimer’s disease.

Merck’s investigational Alzheimer’s treatment–called MK-8931–targets a substance in the brain called amyloid. Scientists have hypothesized that the buildup of amyloid in the brain plays a role in Alzheimer’s disease. A number of major pharmaceutical companies have been looking for a treatment to stop the progression of the disease, which impairs memory and cognitive skills in the elderly.

by IBN Live:

A drug intended for diabetes appears to restore memory in brain cells affected by Alzheimer’s disease, researchers say. Medical researchers at the University of Alberta led by Jack Jhamandas took brain tissue from animal models with Alzheimer’s disease and tested the tissue in the lab, looking specifically at the cells’ memory capacity.

When brain cells are shocked by a barrage of electrical impulses, the cells “remember” the experience, which is a typical way to test or measure memory in the lab setting. Amyloid protein, which is found in abnormally large amounts in the memory and cognition parts of the brains of Alzheimer’s patients, diminishes memory.

A sister protein, known as amylin, which comes from the pancreas of diabetic patients, has the same impact on memory cells. Jhamandas and his team demonstrated last year that a diabetes drug that never made it to market, known as AC253, could block the toxic effects of amyloid protein that lead to brain-cell death.

by Ransdell Pierson and Debra Sherman for Reuters:

Merck & Co Inc has moved to the forefront of Alzheimer’s disease research by starting a mid-stage study of a drug from a new class of oral medicines that aim to shut down production of a protein associated with the memory-robbing disease.

The drugmaker said on Monday it had started the trial to evaluate the safety and effectiveness of its so-called BACE inhibitor, named MK-8931, in patients with mild-to-moderate Alzheimer’s disease.

The Phase II trial, which will compare the drug with a placebo, is a global, multi-center study that includes a group of 200 patients to test safety. The study is expected eventually to enroll up to 1,700 patients in the main Phase III trial.

Darryle Schoepp, head of neuroscience at Merck, said drugmakers have been trying for a decade to develop treatments that arrest Alzheimer’s disease by blocking beta secretase, an enzyme involved in production of toxic beta amyloid proteins that form plaque in the brain believed to be a contributor to Alzheimer’s disease.

by Melissa Healy for Los Angeles Times:

A biological medication already widely used to treat plaque psoriasis may be able to slow the accumulation of amyloid plaques in the brain that are the hallmark of Alzheimer’s disease, a new study has found. The same study found that in older mice with established Alzheimer’s, this treatment approach, which suppresses the brain’s immune reaction to beta amyloid, brought a marked improvement in cognitive function and may even halt or reverse early signs of Alzheimer’s.

The new study was published this week in the journal Nature Medicine.

Conducted by researchers in Switzerland and Germany, the study offers a glimmer of hope in the thus-far discouraging search for a therapy that could halt or reverse the inexorable process of neuronal loss and mental decline that affects some 35-million people worldwide. It also strengthens evidence for the long-suspected role of inflammation in the development of Alzheimer’s disease.

by Sean Patterson for WebProNews:

A new study shows that a drug used to treat insulin resistance in diabetics could improve cognitive performance in some people with Alzheimer’s disease.

In the study, published this week in the Journal of Neuroscience, the drug rosiglitazone was used on mice that have been genetically engineered to serve as models for Alzheimer’s disease. Researchers found that treatment with the drug improved learning and memory in the mice, while it also normalized insulin resistance.

The researchers believe that the drug reduced the negative influence of Alzheimer’s on a brain-signaling molecule called extracellular signal-regulated kinase (ERK). ERK becomes hyperactive in the brains of Alsheimer’s patients when they begin to exhibit mild cognitive impairment. This leads to improper synaptic transmission between neurons. The study shows that the drug activates the peroxisome proliferator-activated receptor gamma (PPARy) pathway in the brain, reducing ERK activity.

by Science Blog:

Researchers at Dalhousie University have discovered a new technique using “computer-aided” drug design that may lead to an entirely new approach in the treatment of Alzheimer’s disease (AD).

“Alzheimer’s is a devastating disease for which no truly disease-modifying drugs are available. Our approach is completely novel. We explore how the human body attempts to protect itself from Alzheimer’s, and then we exploit this to develop an entirely new approach to therapeutics,” explained Dr. Weaver, a professor at Dalhousie University, clinical neurologist at Capital Health and IWK Health Centre, Canada Research Chair in Clinical Neuroscience, and the DMRF Irene MacDonald Sobey Chair in Curative Approaches to Alzheimer’s Disease. “We are extremely excited about the results presented in this paper and believe that this may represent a new approach to the treatment of AD.”

Weaver says that he and his fellow researchers have successfully identified molecules that are able to prevent the disease-producing aggregation of both beta-amyloid and tau – the two proteins whose misfolding is implicated in the causation of Alzheimer’s.