A new drug shows promising results: Early results indicate that the drug could reverse natural, age-related cognitive decline. Researchers also believe that it might help patients whose memories are impaired because of conditions such as depression, schizophrenia and Alzheimer’s disease.
Interesting, the video on the page in the link for today highlights life style changes while the words on the site talk about a new compound that has been found that could prevent Alzheimer’s. Both are interesting to read/watch.
It has been known that people can be disoriented after general anesthesia but now a study found that propofol (a very common drug to use) also disrupts presynaptic mechanisms, probably affecting communication between neurons across the entire brain in a systematic way that differs from just being asleep. In this way it is very different than a sleeping pill
In a new study, a Salk team found that J147 binds to a protein called ATP synthase, which is responsible for producing a common cellular “energy currency” known as ATP. This protein is known to control aging in worms and flies, and the researchers found that by binding to it the drug was able to prevent age-related damage to the brain.
Novel Drug Shows Promising Results in Alzheimer’s Model
Scientists report that a novel small-molecule drug, which works by stopping toxic ion flow in the brain that is known to trigger neuronal apoptosis, can restore brain function and memory in a mouse model of Alzheimer’s disease (AD). The team believes the drug could be used to treat AD and other neurodegenerative diseases such as Parkinson’s and amyotropic lateral sclerosis (ALS).
You would think that all would be working cooperatively towards a solution for Alzheimer’s but this is not the case. The ridiculous costs and time that it takes to run effective tests lead to a short time to recoup your research costs when you would find a workable solution. Researchers can not make a good case that this is a wise investment for Pharmaceutical companies.
So something is really wrong here and the government should look into this.
Buildups of “clumpy” proteins in the brain are well-known hallmarks of Alzheimer’s, but not everyone who has them goes on to develop this neurodegenerative disease. Why is that? New research investigates.
Dr. Debbie Toiber, of the BGU Department of Life Sciences, and her team discovered that a specific protein — Sirtuin-6 (SIRT6) — is severely reduced in the brains of Alzheimer’s patients. SIRT6 is critical to the repair of DNA, the deterioration of which “is the beginning of the chain that ends in neurodegenerative diseases in seniors,” she explains.
The blood-brain barrier prevents us from simply being able to inject the protein into the brain to replenish its supply. Dr. Toiber is currently working on finding a way to increase the expression of the protein into the brain.
Ionis and Biogen are bringing to bear the Ionis drug technology called antisense, which targets diseases processes at the genetic level. It blocks or modifies production of proteins involved in disease.
The Phase 1/2a study of the Alzheimer’s drug, IONIS-MAPTRx, seeks evidence of safety and signs of activity. It’s to be given in 44 patients with mild Alzheimer’s over three months.The drug targets microtubule-associated tau protein, also called MATP, or tau, an abnormal protein associated with Alzheimer’s.
As a first step, a team is testing whether it’s possible to stop or slow tau-driven neuron loss and inflammation by lowering ApoE in the early life of laboratory rodents. This scheme mimics a human scenario better than the recent study, which analyzed mice that express or lack APOE from birth. “The implication here, with the recent tau findings, is that you’d really block the neurodegeneration that leads to cognitive decline,” Holtzman says.
Nearly three dozen new Alzheimer’s drugs may reach the market in the next five years, researchers say.
That includes 27 drugs in phase 3 clinical trials, which are later in the drug review process. It also includes eight drugs in phase 2 clinical trials, according to an analysis by ResearchersAgainstAlzheimer’s (RA2) investigators, an UsAgainstAlzheimer’s network.
Drugs used to treat acid reflux and ulcers don’t appear to boost the risk of dementia, as has been previously suspected, new research suggests.
The study focused on widely used proton pump inhibitors (PPIs) drugs — medicines such as Prevacid, Prilosec and Nexium. Previous studies have suggested the drugs may increase the risk of dementia and Alzheimer’s disease in people aged 75 and older.
An InSysBio scientific group led by Tatiana Karelina has developed a quantitative system pharmacology model of Alzheimer’s disease. The first part has been published in CPT Pharmacometrics & Systems Pharmacology, and shows how to design initial phases of clinical trials of new drugs and to interpret the data.
The joint effort, known as the Alzheimer’s Combination Therapy Opportunities (ACTO) grant initiative, will provide $2 million this year for testing approaches that simultaneously target two or more processes believed to underlie, exacerbate, or occur in the disease.