{"id":3312,"date":"2016-10-25T18:09:04","date_gmt":"2016-10-25T18:09:04","guid":{"rendered":"https:\/\/braintest.com\/?p=3312"},"modified":"2019-12-06T18:00:24","modified_gmt":"2019-12-06T18:00:24","slug":"alzheimers-news-highlights-developments-2015","status":"publish","type":"post","link":"https:\/\/braintest.com\/es\/alzheimers-news-highlights-developments-2015\/","title":{"rendered":"Alzheimer’s News \u2014 Highlights and Developments in 2015"},"content":{"rendered":"

When looking at the bigger picture, Alzheimer’s<\/a> is still in many ways, a mystery.<\/p>\n

With that being said, each year, researchers make some impressive discoveries, unlocking clues that will hopefully lead to long-term solutions. With more than 40 million people currently living with this disease worldwide, breakthroughs are not only exciting \u2014 they can be life-changing.<\/p>\n

Throughout the years 2015 and 2016, there’s no doubt that progress has been made and although research sometimes creates more questions than answers, it’s clear that discoveries are becoming more reliable and concrete. To recap, here’s some of the most impressive findings that have been recently published.<\/p>\n

Breakthrough Research In the Year 2015 <\/strong><\/p>\n

With so many researchers dedicating their life’s work to Alzheimer’s, there’s no doubt that progress is being made. Here are some of the most memorable and encouraging studies published last year:<\/p>\n

\u201cAlzheimer’s Treatment Fully Restores Memory Function\u201d <\/em><\/strong><\/p>\n

An Australian study<\/a>, published in Science Translational Medicine<\/em>, found that scanning ultrasound has the ability to remove amyloid-\u03b2, helping to restore memory function in mice. These protein pieces are what clump together, resulting in plaques \u2014 abnormal clusters that build up between the brain’s nerve cells.<\/p>\n

Within this study, scientists were interested in removing amyloid-\u03b2 from mice through the use of scanning ultrasound \u2014 a noninvasive method with possible therapeutic effects. When using this method, plaques were cleared in 75 percent of the scanning ultrasound-treated mice. In turn, it was found that these treated mice showed improved performance on three memory tasks.<\/p>\n

 <\/p>\n

\u201cResearchers May Have Discovered the Cause of Alzheimer’s\u201d<\/em><\/strong><\/p>\n

Without understanding the true cause of Alzheimer’s, it’s tough to come up with effective treatment options. Back in April 2015, researchers discovered a possible cause<\/a> \u2014 one which may lead to new treatments. While studying mice, it was found that certain immune cells play a vital role. These cells, known as microglia, are stained black and shown below.<\/p>\n

Although these immune cells typically protect the brain, within Alzheimer’s disease, it appears that they begin to abnormally consume arginine \u2014 an important nutrient. Published in the Journal of Neuroscience<\/em>, it was found that when blocking microglia and arginase, an enzyme that breaks down arginine, fewer plaques developed.<\/p>\n

Due to this enzyme, as well as the blood-brain barrier, simply eating more arginine would not resolve this issue. Of course, this specific research is still in its early stages, however, it does shed some light on potential causes and significant risk factors. It is research like this, that is opening the doors to new ideas regarding the progression of Alzheimer’s.<\/p>\n

\u201cNaturally Occurring Molecule May Delay Alzheimer’s Onset\u201d<\/em><\/strong><\/p>\n

When studied in mice<\/a>, researchers found that a molecule which occurs naturally in humans, may be able to delay processes that lead to Alzheimer’s. Long before symptoms surface, in the earliest stages of Alzheimer’s, proteins in the brain begin to build up. Although slow to begin, this process rapidly turns into a chain reaction, causing these clumps to spread across the brain.<\/p>\n

Published in Nature Structural & Molecular Biology<\/em>, researchers found that Brichos \u2014 a human molecule, essentially stops the formation of amyloid fibrils into clumps. Although this molecule does not stop the initial formation, it does inhibit a chain reaction. After injecting mice with both amyloid proteins and Brichos, their brains appeared to be protected against this catalytic cycle.<\/p>\n

Although it was shown to reduce toxicity and help maintain protein homeostasis, researchers admit that Brichos would not likely be a suitable drug, as it would be absorbed by the body before reaching the brain, but it does provide a starting point. It is their goal to search for molecules that provide a similar effect, potentially developing a new therapy option in the future.<\/p>\n

Breakthrough Research In the Year 2016 <\/strong><\/p>\n

\u00a0<\/strong><\/p>\n

The year 2016 isn’t quite through, yet researchers have been able to make some significant progress the past ten months or so. Building off of past research, scientists continue to make progress, as they search for a potential cause and cure. Here are some of the highlights that have been published so far, in the year 2016.<\/p>\n

 <\/p>\n

\u201cAn Antibody Has Been Shown to Clear Toxic Amyloid Plaques\u201d <\/em><\/strong><\/p>\n

Just recently, this study<\/a> was published in Nature<\/em>, showcasing the positive effects of aducanumab \u2014 a human antibody. After a year, individuals with Alzheimer’s, who received the highest doses of the antibody, displayed virtually no build up of amyloid plaques.<\/p>\n

These findings have led scientists to believe that these distinct plaques are not a byproduct, but are at least part of the cause. The brains of these participants were scanned throughout the course of the study, showcasing the progression of a placebo group, as well as three dose groups.<\/p>\n

After one year, the images of the placebo group remained largely unchanged. For those who received a monthly dose of aducanumab, however, they displayed a significant reduction in amyloid plaques. These effects were based on a dose and time-dependent manner \u2014 the higher the dose, the greater the degree of reduction.<\/p>\n

 <\/p>\n

\u201cLost Memories May Be Recovered\u201d<\/em><\/strong><\/p>\n

Based on a recent MIT study<\/a>, it’s believed that memories lost to Alzheimer’s, could potentially be restored. Published in Nature<\/em>, it was stated that in the early stages of Alzheimer’s, mice can form new memories just as well as normal mice \u2014 they just cannot recall them days later.<\/p>\n

Although memories appear to be lost, they are still there \u2014 it’s just a matter of retrieving them. After stimulating new connections between the entorhinal cortex and hippocampus, impaired mice regained the memory in question (the fear of a foot shock). This was achieved using light, stimulating cellular growth.<\/p>\n\n\n\n\n
\u00a0<\/td>\n<\/tr>\n
 <\/td>\n <\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

Unfortunately, this method is too invasive to be used within human subjects. Researchers admit that although the technique, known as optogenetics, cannot currently be used in humans, their research does provide a proof of concept. It is possible that future technology will be able to both activate and inactivate specific cells deep within the brain.<\/span><\/p>\n

\u00a0<\/em><\/strong><\/p>\n

\u201cCannabinoids Remove Alzheimer’s Proteins From the Brain\u201d<\/em><\/strong><\/p>\n

Since the initial launch of the War on Drugs <\/em>in the 1970s, cannabis has developed a negative reputation, despite its potential medicinal benefits. Early this year, researchers found that THC and other compounds found in the cannabis plant, may help remove amyloid beta from the brain. More specifically, the activation of cannabinoid receptors may inhibit neural toxicity.<\/p>\n

This is not the first study to report the potential neuroprotective effect of cannabis, however, it is the first to demonstrate the positive effect on both amyloid beta accumulation and inflammation in nerve cells. Published in Aging and Mechanism of Disease<\/em>, researchers were able to show that intracellular amyloid beta, initiates a toxic inflammatory response, resulting in cellular death.<\/p>\n

 <\/p>\n

References<\/strong><\/p>\n

http:\/\/stm.sciencemag.org\/content\/7\/278\/278ra33<\/a><\/p>\n

http:\/\/jneurosci.org\/content\/35\/15\/5969.short<\/a><\/p>\n

http:\/\/www.nature.com\/nsmb\/journal\/v22\/n3\/full\/nsmb.2971.html<\/a><\/p>\n

http:\/\/www.nature.com\/articles\/nature19323.epdf<\/a><\/p>\n

http:\/\/www.nature.com\/nature\/journal\/v531\/n7595\/full\/nature17172.html<\/a><\/p>\n

http:\/\/www.nature.com\/articles\/npjamd201612<\/a><\/p>\n\r\n\t

\r\n\t
Subscribe & keep up to date on Alzheimer's, Dementia & more<\/section>\t\t\t
\r\n\r\n\t\t\t\t\t\t\t\t\t\t\t\t\t