VIDEO: Alzheimer's breakthrough in Melbourne drug trial

[Confounding]

More promising news.

VIDEO: Alzheimer's breakthrough in Melbourne drug trial

 

[Eaglewings]

I hope this continues to work and heal the minds of so many suffering from this horrible disease.



.

 

[waltky]

Loss of Y chromosome linked to Alzheimer's in men over 80...

Study links loss of Y chromosome to Alzheimer’s in men
Wed, May 25, 2016 - About one in five men aged over 80 lose the Y chromosome from their blood cells, and this condition has now been linked to an increased risk of Alzheimer’s disease, researchers said on Monday.

The condition known as loss of Y (LOY), is the most common genetic mutation acquired during a man’s lifetime. Previous research has shown LOY can raise the likelihood of cancer and is more frequently found in smokers. Researchers now think the condition might serve as a predictive biomarker for a wider range of health problems. For the study in the American Journal of Human Genetics — led by Lars Forsberg and Jan Dumanski of Uppsala University in Sweden, along with colleagues in Britain, France, the US and Canada — researchers examined LOY cases in more than 3,200 men with an average age of 73.

About 17 percent showed LOY in blood cells. Those who had been already diagnosed with Alzheimer’s had a higher degree of LOY, they found. Also, those who had not yet been diagnosed with dementia, but had LOY were more likely to develop Alzheimer’s in subsequent years. “Having loss of Y is not 100 percent predictive that you will have either cancer or Alzheimer’s,” Forsberg said. Some men with LOY in the study lived with no symptoms well into their 90s. “But in the future, loss of Y in blood cells can become a new biomarker for disease risk and perhaps evaluation can make a difference in detecting and treating problems early,” Forsberg said.

University of California, San Francisco, professor of medicine Chris Lau said that the study sheds little light on why Alzheimer’s risk might be elevated in these men. “Although informative, the study is preliminary in nature and only highlights the fact that the Y chromosome could serve important functions beyond male sex determination and sperm production,” said Lau, who was not involved in the study. “What exactly on the Y chromosome that increases the risk of Alzheimer’s disease is the key issue,” he said.

Since the Y chromosome contains many genes — some unique to men and others shared with women, who do not have a Y chromosome — more research is needed. “It depends on what is lost to determine what is important for Alzheimer’s disease. Without such information, the loss of Y is just an observation,” Lau said.

Study links loss of Y chromosome to Alzheimer’s in men - Taipei Times

 

[waltky]

Allosteric ligands, targets a protein that is involved with memory...

New Alzheimer's Drug Slows Memory Loss, Extends Life in Mouse Model
December 19, 2016 - According to the Alzheimer's Association, an estimated 47 million people worldwide have been diagnosed with Alzheimer's disease, a neurodegenerative condition that causes severe dementia.

But researchers — originally at the University of Leicester in England, but now at the University of Glasgow in Scotland — have found a new class of drug that not only slows memory loss, but appears to restore it and to extend life in a mouse model of Alzheimer's. The drug, called allosteric ligands, targets a protein that is involved with memory. As patients with Alzheimer's deteriorate, the protein in a brain region called the hippocampus becomes less active. However, the experimental drug appears to activate the protein, called the M1 muscarinic receptor, which improves memory.

A patient prepares for a PET scan as part of a study on Alzheimer's disease at Georgetown University Hospital in Washington​

Andrew Tobin, professor of molecular biology at the University of Glasgow, is lead author of the work, which was published in the Journal of Clinical Investigation. For reasons that are not entirely clear, Tobin says the drugs also extended the life of the mice. "[The drug is] still going through this [memory protein], but it's doing something else in the brain which is protecting the neurons from neurodegeneration,” he said. “And the big question that we have in the lab is, ‘What is that mechanism? What is the biochemical mechanism that underlies that response?’ And, of course, that's the next thing we'll be looking at." Current treatments for Alzheimer's disease are designed to ease symptoms, while researchers say their work represents an actual treatment.

The experimental compound was tested in a mouse model of Alzheimer's. The animals were bred to exhibit signs of mad cow disease, which looks similar to Alzheimer's in humans in terms of memory loss, progression and death. On a memory test, the untreated mice were unable to recall receiving a mild electric shock, while the treated mice did remember the stimulus. Tobin cautions that a drug is probably five to 10 years away. "These advances take us forward a step at a time,” he said. “So whereas they do give a lot of hope, … it's not an immediate cure.”

New Alzheimer's Drug Slows Memory Loss, Extends Life in Mouse Model

 

[MarathonMike]

I hope it's true I've been reading about breakthroughs on Alzheimer's for years.

 

[waltky]

Uncle Ferd says dey oughta test it on Granny...

Breakthrough Drug Restores Brain Function in Alzheimer’s Animal Model – Large-Scale Clinical Trial Now Planned
July 28, 2017 - Scientists from the Technical University of Munich have published a new paper showing that using a BACE inhibitor drug reduces the amount of amyloid beta in the brains of mice and restores the normal function of nerve cells and significantly improves memory.

Amyloid beta is a protein believed to be a major cause of Alzheimer’s disease and significant research around the world has focused on finding ways to remove or reduce the accumulation of amyloid beta in the brain. No drug on the market today can effectively treat Alzheimer’s disease and with 50 million already suffering from Alzheimer’s globally and tens of millions more projected to be diagnosed with the disease as the global population ages in the coming decades, it’s becoming a serious concern for governments and policy makers.

This new study led by Dr. Aylin Keskin, tested a substance that inhibits beta secretase in a mouse model of Alzheimer’s disease. The mice used in the study accumulate large amounts of amyloid beta, which then become amyloid beta plaques in the brain and lead to cognitive decline. The mice were feed the beta secretase inhibitor for up to eight weeks, after which the scientists examined the brains of the mice using an imaging technique known as two-photon microscopy to see the details of individual nerve cells.

Amyloid-β plaques (blue) and nerve cells (green) in the brain of an Alzheimer mouse model.​

The brains of the mice in the study showed amyloid beta and brain functions actually normalized. The brains showed less hyperactive nerve cells, and the slow-wave brain patterns looked like patterns found in healthy mice. A major discovery from the study was that the memory of the mice significantly improved and they were able to remember and location of a hidden platform in a water-filled maze as fast as healthy mice. “What really impressed and amazed us was the reversibility of the symptoms. Before the treatment, the mice had a marked clinical picture with amyloid beta plaques in their brain. Nevertheless, the substance was able to restore important brain functions and abilities,” said Dr. Keskin.

Clinical trials in humans

The results from the study will soon be trialed in human Alzheimer’s patients with a large-scale clinical trial currently being planned with around 1000 participants that will test a modified form of the BACE inhibitor drug. Co-author of the study, Dr. Marc Aurel Busche said “Needless to say, we very much hope that the promising discoveries in the animal model will translate to humans.”

Breakthrough Drug Restores Brain Function in Alzheimer's Animal Model - Large-Scale Clinical Trial Now Planned

See also:

Gene Editing Has Successfully Treated Muscular Dystrophy in Dogs – Human Trials Next
July 26, 2017 - In new research published on Monday, an international team of researchers report that they have been able to reverse the symptoms of Duchenne muscular dystrophy in dogs using a single injection of a novel gene therapy.

The symptoms of the disease did not return in the dogs for the two year duration of the study. Duchenne muscular dystrophy is a severe from of muscle wasting disease that affects one in 5000 males at birth and the average expectancy of patients is 26 years. The disease is genetic and caused by mutations that disrupt the production of dystrophin, which is required for muscles to function properly. The team comprised of researchers from Genethon, the AFM-Telethon laboratory, Inserm (UMR) and the Royal Holloway University of London said in a statement that these results are “paving the way for human clinical trials.”

The researchers created a novel gene transfer therapy that restores the dystrophin expression. They injected the dogs with with the gene microdystrophin, a compressed version of the dystrophin gene. Researchers had previously been unable to successfully use the dystrophin gene in gene therapy due to its relatively large size of 2.3 million base pairs. After a single injection the dogs in the study demonstrated “significant restoration of muscle function with a stabilisation of clinical symptoms for more than two years after injection,” said the team.

This is “really a very exciting study indeed”, said Geneticist Darren Griffin of the University of Kent. “The disease has long been a target for gene therapy and it is only to be hoped that sufficient funds can be awarded for this research to reach its natural conclusion and go into full clinical trials,” he said, quoted by the AFP. Muscle weakness caused by Duchenne muscular dystrophy usually appears around the age of four in boys and advances rapidly leaving most unable to walk by the age of 12. Few patients of Duchenne muscular dystrophy survive into their 40s.

Gene Editing Has Successfully Treated Muscular Dystrophy in Dogs - Human Trials Next

Related:

Scientists Regenerate Retinal Cells and Restore Vision in the Eyes of Adult Mice Using Gene Activation
July 28, 2017 - A group of scientists from the University of Washington have shown in new research published in Nature that they can regenerate the retina cells in the eyes of adult mice.

The research may one day make it possible to regenerate the retina cells in eyes of patients with age-related macular degeneration, glaucoma and other pathologies of the eye. The cells of our retinas lack the stem cells that some tissues have that allow them to divide and regenerate. Because of this, damage to the retina is often untreatable with today’s medicine and leads to permanent vision loss.

The scientists created a mouse that had a version of a gene known as Ascl1, the gene enables cells called Müller glia to regenerate damaged retinas. The Ascl1 gene was activated with an injection of the drug tamoxifen. Previous research by the scientists had shown that the Ascl1 gene would only lead to regeneration of the retina if activated within two weeks of the mice birth. The new paper published on Wednesday, demonstrates that that, by using a drug that blocks epigenetic regulation called a histone deacetylase inhibitor, it enables the activation of the Ascl1 gene in the eyes of adult mice.

The Müller glia cells are then able differentiate into functioning interneurons. The paper shows that these interneurons then propagate into the mice retina, forming connections with other retinal cells, and react normally to signals from the light-detecting retinal cells. The lead researcher of the team, Prof. Tom Reh said in an interview with the University of Washington Health Science NewsBeat they hope to discover if other factors exist that can be activated to allow the Müller glia cells to regenerate into all the different cell types of the retina.

Scientists Regenerate Retinal Cells and Restore Vision in the Eyes of Adult Mice Using Gene Activation

 

[sealybobo]

I hope this continues to work and heal the minds of so many suffering from this horrible disease.



.

I sometimes think it'll suck if they come up with a cure so soon after my mom died from Alzheimer's but then what about me my brother and his sons? We have that gene in us so good speed on finding a cure.

Next Sunday will be 1 year. No one knows what it's like unless you care for someone going through it. Horrible.

 

[waltky]

Deep brain stimulation (DBS) therapy acts as a pace maker for Alzheimer's patients..

Brain 'pacemaker' for Alzheimer's
30 Jan.`18 - LaVonne Moore has Alzheimer's disease, but her doctors hope her dementia symptoms could possibly be kept in check by a new type of treatment.

Electric wires implanted deep in her brain stimulate areas involved with decision-making and problem-solving. Unlike many long-term dementia patients, LaVonne, 85, can cook meals, dress herself and organise outings. But it remains unclear whether her deep brain stimulation (DBS) therapy is responsible for her independence. DBS is already helping hundreds of thousands of patients with Parkinson's disease to overcome symptoms of tremor, but its use in Alzheimer's is still very experimental.

Scan showing the implanted wires​

Only a small number of DBS studies have been done for Alzheimer's and they have focused on stimulating brain regions governing memory, rather than judgement. But Dr Douglas Scharre and colleagues at the Ohio State University Wexner Medical Center believe their approach, which targets the decision-making frontal lobe of the brain, might help patients keep their independence for longer.

Deep brain stimulation

* Involves permanently implanting very fine wires, with electrodes, into the brain, under anaesthetic
* The wires are connected to a pulse generator (pacemaker) under the skin of the chest wall
* The device delivers electric stimulation to the brain to improve function or reduce symptoms

LaVonne's brain pacemaker was implanted three and a half years ago. Since then, her husband, Tom, from Delaware, Ohio, says her dementia has worsened - but more slowly than he had expected. "LaVonne has had Alzheimer's disease longer than anybody I know, and that sounds negative, but it's really a positive thing because it shows that we're doing something right." Two other patients have had the same treatment as LaVonne, but only one of them appeared to benefit significantly, according to the Journal of Alzheimer's Disease. Experts say it is too early to say if the treatment will help counteract cognitive decline.

Larger trials

Neurosurgery expert Prof Andres Lozano, who has been conducting his own DBS trials in Alzheimer's patients in Canada, said: "We desperately need a novel treatment for Alzheimer's. "This may seem bold and aggressive to some, but it is promising. Studies so far show it is safe. "We've got patients with Parkinson's who have had these devices inside of them for 30 years with no problems. "Although we are not talking about treating the Alzheimer's degeneration, we can look at changing the downstream consequences by turning parts of the brain back on." Dr Carol Routledge from Alzheimer's Research UK, said: "The study did not compare against a dummy treatment and so while signs of benefit are worthy of follow-up, the full benefits and cost-effectiveness of this treatment need much more robust investigation in larger trials."

Brain 'pacemaker' for Alzheimer's