2nd International Conference on Alzheimers, Dementia and Related Neurodegenerative Diseases

As gene regulation changes in Alzheimer’s disease, scientists believe that histone deacetylases (HDACs) go into overdrive, shutting down transcription of certain genes. Consequently, several research groups are exploring the potential of HDAC inhibitors as AD therapeutics, with at least two trials currently enrolling. The recent development of a PET tracer that recognizes class I HDACs in the brains of living people provides a valuable tool for such trials. Now, however, the first HDAC PET data from people with AD upends previous findings. Tharick Pascoal of McGill University, Montreal, reported that HDAC levels drop as disease advances. “That was a surprise to us. We expected the opposite result,” Pascoal told Alzforum. At first, the researchers worried that there might be errors in their methodology; however, validation by a second group studying an independent cohort convinced them the finding was real, and robust. “I’ve never seen two independent PET studies where th

Could light and noise treatments effectively treat Alzheimer’s disease? This neuroscientist thinks so. The quest for ways to prevent and treat #Alzheimer’s disease has led scientists to explore a wide variety of techniques. One that has been especially interesting is the use of flickering lights, which has been shown to reduce levels of #amyloid-beta plaque in the brains of mice. Is this finding, as well as those using pink noise (a mixture of high and low frequencies that is more natural and balanced than white noise), a door to a whole new way to treat Alzheimer’s disease and other neurological conditions? Li-Huei Tsai, a neuroscientist at Massachusetts Institute of Technology, is one of a growing number of #scientists who believe it is. She and her colleagues noted that exposure to a strobe light tuned to 40 hertz has cleared amyloid-beta from the brain. This approach is an example of how brainwave manipulation may be a new way to delay, treat, or even reverse neurol

A possible medical breakthrough. New research is helping doctors understand what causes Alzheimer’s in women, the majority of Alzheimer's patients . As 13WHAM’s Samantha Miles reports, women who’ve had miscarriages may be at a higher risk for developing the disease. Dina Johnson knows the challenges of Alzheimer’s. “Not only do I see it, I’ve experienced it as a caregiver,” said Johnson. She's also lost family to dementia . She often worries her kids will develop it. “I have three girls, right? I’m young. I’m only in my 40s, so I think about the risk they may go through in the future.” The same study also showed women who had three or more children had a 12 percent lower risk of developing dementia .

A clinical-stage biopharmaceutical company announced 2 clinical milestones related to ACI-24, an anti-Abeta vaccine candidate against Alzheimer's disease and the Abeta-related cognitive decline in Down Syndrome. ACI-24 is a liposomal therapeutic anti-Abeta vaccine candidate, which generates antibodies specific to disease-causing conformations.  The vaccine is designed by AC Immune to stimulate a patient's immune system to produce antibodies that specifically target the oligomeric and fibrillary Abeta proteins, to prevent plaque accumulation and to enhance plaque clearance. Andrea Pfeifer, the CEO of AC Immune, said in a press release, "We are delighted with the progress of ACI-24, which is currently the only clinical-stage vaccine targeting the associated Abeta-induced cognitive decline in people with Down Syndrome.” “Vaccines are potentially an important option for the treatment and prevention of neurodegenerative diseases ."

Having a relative with Alzheimer’s disease can be difficult to cope with and the situation is likely to be mutual. The degenerative condition leaves many patients feeling lost and disorientated, but it can be hard to understand what it’s really like when you’ve never experienced it. Now, a US company has developed a virtual reality (VR) headset that mimics the disease for users. Embodied Labs hopes that the device will help to foster empathy in relatives and caregivers, because they’ll have first-hand knowledge of what it’s really like. Carrie Shaw, creator of the device at Embodied Labs, told Chicago magazine: “We see that people have better understanding after going through the Alzheimer’s experience that it’s a disease of the brain, and that when people are acting out it’s because of their disease and not because of their personality or intentional behaviour.” Stepping away from traditional lectures and textbook learning could be the future for healthcare professi

Many everyday things have been proposed to cause Alzheimer’sdisease over the years deodorant, dental fillings, diet soda, and flu shots, to name just a few. But none of these proposed causes has stood up to sustained scientific scrutiny, and the alarm bells raised by early research have turned out to be false alarms. Specifically, according to NBC, “Women who had three kids had a lower lifetime risk of Alzheimer’s than women who had one child, researchers found.” The implications for women who have fewer children is clear: This decision may increase the risk of Alzheimer’s disease later in life. But is this new culprit–based on an observational study of about 15,000 women reported at the Alzheimer’s Association conference in Chicago–any more likely to be guilty than the previous suspects? Stephen Soumerai, ScD, Professor of Population Medicine at Harvard Medical School and Harvard Pilgrim Health Care Institute, says it is way too soon to know.

Researchers from Boston University School of Medicine, in collaboration with scientists from the Alzheimer’s Disease Sequencing Project (ADSP), have discovered new genes that could contribute to the onset of Alzheimer’s disease. The new discovery may advance precision medicine treatments for the degenerative condition.   The National Institutes of Health developed ADSP in response to the National Alzheimer’s Project Act, which aims to improve health outcomes and reduce financial burdens for individuals with Alzheimer’s . Alzheimer’s is the leading cause of dementia and the sixth leading cause of death in the US. However, despite the growing prevalence and rising costs of the condition, the genetic and environmental factors that make some individuals more susceptible to this disease are still not well understood. “This is a critical time in Alzheimer's research, with new opportunities to build upon what we have learned,” Richard J. Hodes, MD, Director of the Na

The long, discouraging quest for a medication that works to treat Alzheimer’s reached a potentially promising milestone. For the first time in a large clinical trial, a drug was able to both reduce the plaques in the brains of patients and slow the progression of dementia . More extensive trials will be needed to know if the new drug is truly effective. “This trial shows you can both clear plaque and change cognition,” said Dr. Reisa Sperling, director of the Centre for Alzheimer Research and Treatment at Brigham and Women’s Hospital in Boston, who was not involved in the study. “I don’t know that we’ve hit a home run yet. It’s important not to over-conclude on the data. But as a proof of concept, I feel like this is very encouraging.” Aside from a couple of medications that can slow memory decline for a few months, there is no effective treatment for Alzheimer’s , which affects about 44 million people worldwide, including 5.5 million Americans. It is estimated that those

Mental confusion, sleeplessness and mood swings have all been linked to Alzheimer’s disease , but the health of your eyes could also be a predictor, according to a new report. Researchers from the University of Washington School of Medicine recently conducted a study, published in the journal Alzheimer’s &Dementia , to explore eye conditions that may be associated with the brain illness. To do so, they examined 3,877 adults aged 65 and older who were a part of the Adult Changes in Thought database. During the five-year trial, which began in 1994, about 800 of the subjects were diagnosed with Alzheimer’s .   “This study solidifies that there are mechanistic things we can learn from the brain by looking at the eye.” A better understanding of neurodegeneration in the eye and the brain could help diagnose Alzheimer’s early, but they said the connections need to be investigated more.  The main message from this study is that ophthalmologists should be more a

The Alzheimer's disease research community is in a great deal of flux at the moment. After a series of high-profile clinical trial failures, rages over whether the current causal hypothesis for the disease is correct. A new study has revealed novel insights into the early stages of the disease's development and suggests treatment may only be effective if delivered before a person becomes symptomatic. For several decades the generally agreed hypothesis regarding the main symptomatic cause behind the degenerative effects of Alzheimer's disease was that the build-up of plaques, composed of a protein called beta-amyloid, resulted in the systematic destruction of neurons.  But the big problem that has arisen is that almost all efforts to target this amyloid build up, in one way or another, have failed. An astounding 99.6 percent of clinical trials into drugs to help beat Alzheimer's have failed. Attempting to better explain why amyloid-targeting drugs ar

In the end it will be microbes’ bacteria, viruses and fungus found to be at the root of all disease and aging, and specifically Alzheimer’s , contends geneticist Dr. Rudolph “Rudy” Emile Tanzi. “The two biggest threats to healthy aging have had to do with dealing with infection,” said Tanzi, who specializes in Alzheimer’s and the brain at Massachusetts General Hospital (MGH) and Harvard Medical School. “Think about it. When we increased the lifespan from 35 to 50, it was by covering the sewers. When we increased the lifespan from 50 to 75, it was with the use of antibiotics. Now we are looking for viruses in all of the major life-threatening diseases of our time Alzheimer’s , cancer, Parkinson’s and guess what? Infection is now cropping up in all of them.” And though evidence continues to mount that could prove his theory, Tanzi says scientists are just beginning to scratch the surface of the culprits that can trigger the spiral into Alzheimer’s disease .

In a recent research done in University of Pennsylvania in Philadelphia, it was observed that Alzheimer's disease risk is associated with reduced levels of plasmalogens , a type of phospholipid produced in the liver. They play key roles in maintaining the health of brain cells. From the liver, plasmalogens are carried to the brain and other organs through the blood. Levels of these phospholipids can be measured through specialized tests that have been devised by Dr. Kling in collaboration with colleagues from the Alzheimer's Disease Metabolomics Consortium at Duke University in Durham, NC. The researchers identified three indices — assessing the ratios of different plasmalogens to each other, the ratios of plasmalogens to other lipids, and a combination of these measurements  that allow them to determine the amount of plasmalogen as it relates to cognitive functioning . Specifically, they were interested in confirming whether decreased plasmalogen levels wer

Effective therapeutics to counteract the formation of amyloid plaques in Alzheimer's disease and type 2 diabetes are not yet available. Scientists at the Technical University of Munich (TUM) have now come a little bit closer to a solution: They have described a new class of designed macrocyclic peptides that are highly potent inhibitors of amyloid formation . Amyloid plaques, which are protein deposits, play a crucial role in the development of Alzheimer's disease and type 2 diabetes. Several teams of scientists around the world are working on finding ways to prevent amyloid plaque formation in the human brain. "Therefore, further investigations are now planned to verify whether the MCIPs are also effective in in vivo models. Furthermore, the MCIPs could also be suitable as templates for the development of small molecule peptidomimetics (molecules mimicking peptide chains), which might also find application as anti-amyloid drugs in Alzheimer's and type 2 d

Salk Institute scientists have found preliminary evidence that tetrahydrocannabinol (THC) and other compounds found in marijuana can promote the cellular removal of amyloid beta, a toxic protein associated with Alzheimer’s disease . “Although other studies have offered evidence that cannabinoids might be neuroprotective against the symptoms of Alzheimer’s , we believe our study is the first to demonstrate that cannabinoids affect both inflammation and amyloid beta accumulation in nerve cells,” says Salk Professor David Schubert, the senior author of the paper. THC is responsible for the majority of marijuana’s psychological effects, including the high, due to its natural pain-relieving properties. Salk researchers have found that high levels of amyloid beta were associated with cellular inflammation and higher rates of neuron death. They demonstrated that exposing the cells to THC reduced amyloid beta protein levels and eliminated the inflammatory response from the nerv

Alzheimer’s disease is thought to have a significant link to reduced generation of neurons. To investigate this link, the researchers, led by Yacine Tensaouti, studied the mechanisms involved in the production of new hippocampus neurons, looking at the role of a gene called Apolipoprotein E (ApoE). A variant of this gene, called ApoE4 , is present in 10 to 20% of the human population and is associated with the development of late-onset Alzheimer’s . Mice were genetically modified to either be completely deficient of ApoE, produce human ApoE4, or produce ApoE3 – the most common form of ApoE in humans and not associated with any disease risk. They found that both the ApoE-deficient and ApoE4-expressing mice had severely reduced complexity in their newly produced hippocampus neurons , compared to both normal mice and those which expressed ApoE3. This, they suggest, shows the central role ApoE expression plays in hippocampus neuron growth and development.

Alzheimer's disease is characterized by the formation of amyloid plaques in the brain, which interfere with the normal communication flow between brain cells. These plaques are made out of beta-amyloid amino acids that stick together. Over the past few years, researchers from various institutions have been working to develop antibodies - a type of protein harnessed by the immune system as part of the immune response able to interfere with beta-amyloid and prevent the formation of plaques in the brain . But the search for effective antibodies, though promising, has been riddled with obstacles and setbacks. That is why a team of researchers from Brigham and Women's Hospital in Boston, MA, has recently conducted a series of experiments to identify a better way of targeting beta-amyloid . This, they hoped, would lead to the development of a more efficient antibody to be used in Alzheimer's therapy. Principal investigator Dominic Walsh and team came up with

Astrocytes work to clear so-called amyloid beta proteins from the spaces between neurons, but decades of evidence have shown that if the clearing process goes awry, amyloid proteins pile up around neurons, leading to the characteristic amyloid plaques and nerve cell degeneration that are the hallmarks of memory-destroying Alzheimer's disease . The new study, described Proceedings of the National Academy of Sciences, also reports that the scientists gave drugs called histone deacetylase (HDAC) inhibitors to pH-imbalanced mice cells engineered with a common Alzheimer's gene variant . The experiment successfully reversed the pH problem and improved the capacity for amyloid beta clearance. HDAC inhibitors are approved by the U.S. Food and Drug Administration for use in people with certain types of blood cancers , but not in people with Alzheimer's. They cautioned that most HDAC inhibitors cannot cross the blood-brain barrier, a significant challenge to the direct u

Long-term-care facilities that offer services specifically for people with dementia, including Alzheimer’s disease , could face new state requirements for employee training and “respite care” for caregivers, such as adult day care, should be more clearly defined in Ohio law. Those two proposed changes to state law are the first recommendations of the Ohio House of Representatives’ Task Force on Alzheimer’sand Dementia . The group of 15 elected officials, advocates and other interested parties, led by Rep. Dorothy Pelanda, a Marysville Republican, released its first report in mid-July after gathering testimony from about 30 people last year. The policy specifies several topics to be addressed, including communication skills, pain assessment, medication management, family dynamics, dealing with challenging behaviour and triggers of dementia symptoms . Meanwhile, Ohio is the only state without a comprehensive plan to address the growing problem — something that must change,

Hopes are rising again for a drug to alter the course of Alzheimer's disease after decades of failures. An experimental therapy slowed mental decline by 30 percent in patients who got the highest dose in a mid-stage study, and it removed much of the sticky plaque gumming up their brains , the drug's makers said Wednesday. The results have been highly anticipated and have sent the stock of the two companies involved soaring in recent weeks. The drug from Eisai and Biogen did not meet its main goal in a study of 856 participants, so overall, it was considered a flop. But company officials said that 161 people who got the highest dose every two weeks for 18 months did significantly better than 245 people who were given a dummy treatment . There are lots of caveats about the work, which was led by company scientists rather than academic researchers and not reviewed by outside experts. The study also was too small to be definitive and the results need to be confirme

How does dementia kill you? The disease has been reported as one of the leading causes of death in England and Wales over the last couple of years, but according to an expert, while dementia essentially shuts down the brain, the actual death of a person may be caused by another condition. But can and how does dementia kill you? Dr Andrew Thornber, chief medical officer at Now Patient explained dementia is a terminal illness that shuts down the brain. He said: “The actual death of a person with dementia may be caused by another condition. “People suffering with dementia are likely to be frail toward the end and find it harder to fight off infections and other physical problems due to the progress of dementia . “In many cases death may be hastened by an acute illness such as pneumonia, or complications such as loss of brain function or a heart attack.” It’s important to recognize all the signs of dementia so the patient can receive the best possible care. There are six

The average person with dementia in a nursing home experiences only two minutes of social interaction each day.  A new e-learning program that trains caregivers to engage in meaningful social interaction with dementia patients shows great promise for improving the well-being of the patient, according to a new UK study. “Care home staff are under a lot of pressure — it’s a really tough job. It’s a challenging environment for both residents living with dementia and staff,” said research therapist Joanne McDermid of King’s College London. “Just take a moment to imagine life with just two minutes of social interaction each day,” said Professor Clive Ballard, of the University of Exeter Medical School. “To accept this is discrimination against people with dementia . We urgently need to do better. Most care home training programs are not evidence-based. We know our program works over the long term, and we now know it can be delivered remotely. We now need to roll this out to

The drug, known as BAN2401, targets amyloid, a protein that accumulates in the brain and forms plaques that can compromise nerve cells. It was shown to be successful in slowing the progression of mild cognitive impairment in 856 patients with early Alzheimer’s . “This is the first late-stage, anti-amyloid antibody study to successfully achieve statistically significant results at 18 months, further validating the amyloid hypothesis,” Lynn Kramer, chief clinical officer and chief medical officer with the Neurology Business Group at Eisai, which developed the drug along with Biogen, said according to the Washington Post. According to the Alzheimer Society of Canada , there are currently 564,000 Canadians living with dementia (of which Alzheimer’s is the most common form), and that number is expected to skyrocket to 937,000 in the next 15 years. The annual cost to Canadians to care for those living with dementia is estimated at $10.4 billion.

Scientists in Japan have demonstrated that ultrasound may be useful to stimulate blood vessel and nerve cell formation in the brains of mice.  Dementia affects about 50 million people worldwide, with 10 million new cases occurring every year. There are currently no curative treatments available for vascular dementia or Alzheimer’s disease , the most common causes of dementia . In this study, a team of scientists led by cardiologist Dr. Hiroaki Shimokawa at Tohoku University, Japan, sought a way to treat dementia without using drugs. Shimokawa and his team had conducted previous studies showing that low-intensity pulsed ultrasound (LIPUS) improved blood vessel formation in pigs with myocardial ischemia , a condition where there is reduced blood flow to the heart.  Other studies have reported that LIPUS increases the production of proteins involved in nerve cell survival and growth, in addition to promoting nerve regeneration. Focusing LIPUS treatment on a region in the