Exciting Results from Clinical Trials Prove Monoclonal Antibody Aducanumab Successful in Removing Amyloid

The results of a clinical trial conducted by scientists at Biogen, was recently published in the journal “Nature.” The trial, which lasted for a year, included 165 early-stage Alzheimer’s patients, identified as prodromal or only mildly affected by the disease. The mini mental state examination (MMSE) upon beginning the trial averaged between 23 and 25 across all test groups. The CDR score (clinical dementia) was 1.0 for the mild group and 0.5 for the prodromal group. Researchers wanted to prove the effectiveness of aducanumab, a monoclonal antibody therapy in clearing amyloid (A-beta) plaque from the brain.

The Trial Format

Subjects were divided into five groups according to dose administered: placebo, 1, 3, 6 and 10 milligrams per kilogram of bodyweight. The degree of amyloid removal in patients mildly affected by Alzheimer’s was quite dramatic. The aducanumab antibody did such an efficient job of cleaning the brain of amyloid that the scans of patients who received the highest doses of the antibody were comparable to patients who were defined as having no amyloid.

Side Effectsthe brain

The amyloid clearance results were the most dramatic in the group being given the highest dose (10 mg per kilogram) but the adverse reactions were also the most significant in this group. Overall, the higher the dose, the higher the frequency of adverse events. Those receiving the highest dose experienced as much as a 38 percent adverse rate, which if the drug is approved, would present some challenges to patient managers in treatment over long periods. Lower doses resulted in lower frequencies of adverse events, with only 10 percent needing to be discontinued due to side effects.

Slowing of Cognitive Decline Observed

The degree of cognitive decline during the course of the year was very much tied to the dosage, although there was some decline across all the groups. The placebo group showed the most cognitive decline, slightly less than two points measured by the CDR-SB, whereas those receiving the highest dose showed a cognitive decline of slightly more than .05 points. These results carried over to MMSE too. Once again, the placebo group declined more than 2.5 points by the end of the year, and those receiving 10 milligrams declined around 0.5 points. However, MMSE did not seem to be as dependent upon the dose administered because patients receiving 1 mg were not statistically different than those who received 6 milligrams. These results are similar to the performance of Nilvadipine, small molecule also found to reduce levels of amyloid. Nilvadipine is developed by Archer Pharmaceuticals. A major difference, though, is that Nilvadipine is administered once per day orally, whereas aducanumab must be administered by intravenous injection, one dose per month.
In conclusion, the trial results are good news for Biogen’s researchers. The corresponding reduction in cognitive decline with reduction in amyloid gives further support to the theory that reducing amyloid levels in the brain can be a prevention strategy for Alzheimer’s disease.


New Study Shows Link between Blood Vessel Disease and Alzheimer’s

Study Suggests Possibility of New Risk Factors for Alzheimer’s disease

Though not definitive, a new study recently published in The Lancet Neurology, offers some hope that we might have another tool in our efforts to prevent or diminish the impact of Alzheimer’s dementia.

The study, conducted at Chicago’s Rush University Medical Center, involved analysis of data from post-mortem examinations of the brain cells of 1,143 individuals. The analysis found a link between blood vessel disease and Alzheimer’s, specifically atherosclerosis and arteriosclerosis. The study’s authors stress that at this point, they can only state that there is a link but not the nature of it. For this, more research is needed. Nevertheless, the findings do open up the possibilities of new prevention strategies.

 Alzheimer's disease

Atherosclerosis is when layers of fat enter the vessels, causing a build-up of plaque. Arteriosclerosis is a thickening of the blood vessels. Both are referred to as cardiovascular disease. We have known that stroke is a causative factor in developing dementia but a possible link between blood vessel disease and Alzheimer’s has not been researched. The Chicago study titled, “Relation of Cerebral Vessel Disease to Alzheimer’s Disease Dementia and Cognitive Function in Elderly People; a Cross-sectional Study,” implies that there is such a link.

Scientists examined the brain autopsy data for indicators of Alzheimer’s and of blood vessel disease in the brain. Of the 1,143 deceased individuals, half were over the age of 88 when they died, 42 percent had Alzheimer’s, 35 percent were stricken with arteriosclerosis and 39 percent with atherosclerosis. The research showed that as blood vessel disease worsened, the risk of Alzheimer’s rose. Scientists also found that patients with atherosclerosis demonstrated more severe cognitive dysfunction, especially in the areas of visuospatial abilities, semantic and episodic memory and speed of perception. The presence of APOE ε4, a gene known to be a risk factor for Alzheimer’s, was not compromised in the study.

Clearly, this is a very good beginning and with more research into how blood vessel disease is contributing to Alzheimer’s, we may have yet another way to identify patients at risk and be able to implement earlier and more effective treatment strategies.

Stunning Results: Ten Early Stage Alzheimer’s Patients Recover Memory and Cognitive Functioning

A 69 year old entrepreneur has been suffering from increasing memory loss over the last 11 years, to a point where he was contemplating closing down his business. After six months on a 36-point plan, called metabolic enhancement for neurodegeneration, he began to once again recognize faces, remember his daily schedule, and was able to compute numbers in his head. After a further 16 months on the program, his long-term memory improved to the 84th percentile, and not only does he intend to keep his business open but he has plans for expansion.Doctor examines a patient's tomography

Memory loss in early stage Alzheimer’s patients can be reversed

A remarkable new study coming out of the Buck Institute for Research on the topic of aging is turning how we view Alzheimer’s disease on its head. Conducted in collaboration with the Eastern Laboratories for Neurodegenerative Disease Research at the University of California in Los Angeles, it provides the first evidence that decline in cognitive function and memory loss can be reversed, rocking the foundation of how Alzheimer’s disease is viewed. The study, titled “Reversal of Cognitive Decline in Alzheimer’s Disease”, was published earlier this month in the journal Aging.

APOE4 gene mutation can be overcome

The study included ten patients who had been diagnosed with Alzheimer’s disease, or who were already exhibiting definable mild cognitive dysfunction. Of the ten subjects, nine were carriers of the mutated APOE4 gene, already identified as a risk factor for developing Alzheimer’s. In five cases, both gene copies were mutated, placing these subjects at the highest level of risk. Previous research has shown that in the United States, 65 percent of all Alzheimer’s patients are carrying a mutated APOE4 gene, therefore to see such astonishing results in a research study group with these mutations is very exciting.

According to the study’s author Dr. Dale Bredesen, Professor at the Buck Institute and Easton Laboratories, these results mean that we should no longer ignore the APOE4 mutated gene, assuming it is a fait accompli whether the carrier will suffer from Alzheimer’s. Instead, he says, people should be tested for APOE4 mutation, and if present, placed on a prevention plan as soon as possible.

A 36-point personalized plan may be the key to returning to life

The 36-point plan, or metabolic enhancement for neurodegeneration, includes a number of strategies that impact brain chemistry, such as vitamin supplements, exercise, changes in diet, improved sleep patterns, drugs and brain stimulation activities. The researchers note that this synergistic approach may also improve the efficacy of drug therapies.Elderly couple on seated couch

Another case cited in the new study is of a 66 year old man whose brain scans and neuropsychiatric examinations showed mild cognitive dysfunction. The hippocampus region of his brain, which is critical to learning and memory, was much smaller than normal for a person of his age. The hippocampus region experienced significant growth after 10 months on the 36-point, multi-disciplinary plan.

These remarkable results were not short-lived, as follow-up tests demonstrated that the return to normal cognitive functioning had not diminished.

Bredesen admits that this study involved a small number of patients and that it must be replicated on a larger scale. Nevertheless, the results are “unprecedented” and the improvements in cognitive functioning experienced by test subjects proves that the 36-point, multi-target approach can work.

Michael Mullan at The New College Of Florida

Watch Michael Mullan Speaking at The New College Of Florida :

Less Sugar in Your Diet may Save You from Dementia

Alzheimer’s disease and other Dementia May be Preventable

Sugar Dementia

According to health surveys such as the one reported recently in the Daily Mail Online, an electronic media coming out of the UK, the likelihood of developing dementia or Alzheimer’s rates higher on the fear factor than of developing cancer. Community-wide concern appears to be fueled by the seeming fact that in spite of the tremendous amount of research conducted so far, there is not very much available to treat these diseases. There are drug therapies to help lessen the symptoms and in some cases, to slow down the progression of the disease, but nothing to fully treat it, such as exists for cancers.

The Daily Mail Online article defines dementia as a condition that begins, usually, after the age of 65 impacting roughly one in every six persons over the age of 80. Symptoms include confusion, difficulty putting together thoughts, and memory loss. Altogether, there are in excess of 100 of these dementia, with Alzheimer’s being the most well-known.

The causes of dementia are varied, but Alzheimer’s research demonstrates a definite correlation between the disease and the presence of an over-abundance of amyloid and tau, two deviant proteins which damage the connections between brain cells.

Too much sugar and body fat can place you at a higher risk for dementia
Another common form of dementia is called vascular dementia. In these cases, blood flow is diminished resulting in less blood flowing to the brain cells which in turn results in brain cell death. Blood vessels can become restricted due to stroke or from health conditions, such as obesity and diabetes. Some people will develop a combination of Alzheimer’s and dementia, each one stemming from a different cause. Nevertheless, research has proven that certain proactive steps, such as changing diet and lifestyle, can prevent or at least significantly delay onset of the disease.

For instance, excessive body fat has been linked to dementia. Too much fat tissue in the body causes the release of hormones that destroy brain cells. Too much fat tissue also causes blocked arteries, high blood pressure and cholesterol, known factors in the onset of vascular dementia. Therefore, individuals who maintain a diet high in sugar are not only placing themselves at risk for developing diabetes or obesity, but also for vascular dementia. Scientists have also discovered that blood sugar levels play a role in the signaling process between brain cells, meaning that a high sugar diet places one at risk of developing Alzheimer’s. Diabetes results in damage to the blood vessels, particularly the smaller vessels in the brain, thus impeding cell functioning.

Dementia are not unavoidable

Last March, World Dementia Council head Dr. Dennis Gillings, said that he believes that within five years we will have new treatments for Alzheimer’s and other dementia, even the possibility of halting progression and reversing the damage. In the meantime, Dr. Naji Tabet, a senior lecturer at Brighton and Sussex Medical School and one of the foremost specialists in dementia, told Daily Mail Online that even for those whose family history would indicate they are more likely to develop dementia, there is hope to prevent its onset or significantly delay it, simply by making crucial lifestyle changes such as reducing sugar, maintaining a healthy blood pressure, keeping the body fat index as low as possible, lowering stress and exercising the brain. Dr. Tabet added that what is inevitable is that our brains shrink as we age, and the connections between brain cells become weakened, but if we make these simple lifestyle changes early in life, we can build up a reserve of strength upon which to draw down as aging begins.

Understanding Dementia and Dispelling the Confusion

Dementia is a word that has crept into our everyday vocabulary, but oftentimes it is misused. For instance, we may find ourselves in the middle of a conversation, and suddenly lose our train of thought, or be unable to remember a person’s name. We immediately jump to the conclusion that we are starting to suffer from dementia. However, with all the stress in today’s world, these events could merely be the result of information overload or too much stimulation. Therefore, it is important to understand what dementia is so that the appropriate steps can be taken to address it.

What is dementia?


Dementia, in and of itself, is not a disease. It is a term loosely used to refer to a decline in cognitive functioning—memory, critical thinking, or problem-solving. If the impairment is significant enough to limit your ability to function day to day, then you may be experiencing signs of dementia.
Dementia is not a necessary outgrowth of aging, as is often thought. Alzheimer’s disease is a form of dementia and approximately 60-80 percent of patients with dementia are suffering from Alzheimer’s. Another category of dementia occurs after a stroke, known as Vascular Dementia.

What are the symptoms of dementia?

Dementia symptoms vary from person to person, but to be considered truly dementia, and not some other cognitive interference, at least two of the following outcomes must be present in a significant and constant way:
• Impaired visual perception
• Loss of memory
• Inability to judge and analyze situations
• Problem with communicating and using language
• Unable to focus and give attention to what is before you

Dementia progresses. Usually it begins with small memory losses, such as where you left your keys, or what you were thinking of preparing for dinner. It could be more serious, such as forgetting appointments, paying your bills or the directions to a frequent location. At this stage, an early diagnosis could prevent further deterioration, as well as discover a treatable disease that might be causing the dementia symptoms.

What causes dementia?

Dementia results when there is damage to the brain cells resulting in their inability to communicate. The brain is separated into regions, each one controlling certain physical and cognitive functions. Cells are constantly sending signals to each other, resulting in smooth functioning of the brain and body. When there is an impairment to the cells’ ability to transmit signals, thinking, memory, bodily functions or emotions can be impacted. Alzheimer’s disease, for example, causes an overproduction of certain proteins, which damage the cells’ ability to communicate, thus resulting in the dementia.

How is dementia diagnosed?

Unfortunately, there is not a single test that can be administered to diagnose the presence of dementia. A qualified physician will assess your family medical history, order laboratory tests, conduct a thorough physical exam and analyze your symptoms to arrive at a diagnosis of the type and severity of the dementia.

What can you do if you have been diagnosed with dementia?
Some dementia is treatable and even reversible, depending upon its cause. This is why early diagnosis is so important. Alzheimer’s dementia, however, is not reversible and to date, there are no medicines or treatments that can slow its progression. Significant medical research is ongoing to discover new therapies for Alzheimer’s and other serious dementias.

Can you lower your risk of developing dementia or prevent its onset?
There are some steps you can take to lower your risk of developing dementia, although nothing can completely negate particular risk factors that you may be carrying.
1. Exercise. Exercise causes increased blood flow to the brain which maintains brain cell health.
2. Cardiovascular health. Protect your cardiovascular system by not smoking, keeping your cholesterol level low and watching your weight.
3. Diet. Brain health is also impacted by what you eat. A diet low in fats and proteins, and high in fish, vegetables, nuts, whole grains and fruits, such as the Mediterranean diet, has proven to keep your brain and heart healthy.

Can Alzheimer’s disease be prevented?

New Scientific Hypothesis Brings Hope of Killing Alzheimer’s

More than five million Americans suffer from Alzheimer’s, a devastating neurological disease that robs patients of their memory and cognitive functioning. Finding a prevention tool has been on the wish list of scientists and treatment providers for decades.

Brain-Infecting Microbes: Old Theory Gets a New Lease of Life

Can Alzheimer’s disease be prevented?

A soon to be published editorial in the Journal of Alzheimer’s Disease will re-open an old conversation as to the cause of Alzheimer’s. According to the editorial, signed by 31 scientists from around the world, the cause of the disease may be microbial infections in the brain, such as Herpes simplex virus 1 (HSV-1), Borrelia burgdorferi, which causes Lyme disease, or Chlamydophila pneumoniae, which causes pneumonia. The experts’ theory is that when the APOE є4 gene variant, which is known to be an Alzheimer’s disease risk factor, is present — a microbial infection can cause debilitating damage to the brain. This theory, dismissed once before, is getting a new look, and if researchers are able to prove it, which will not be easy, then perhaps in the future there will be a way to prevent Alzheimer’s disease.

Microbial Infections Vs. Amyloid Proteins and Tau Tangles

To date, researchers have been focusing on amyloid proteins and tau tangles, which have been proven to be causative agents in the brain cell death experienced by Alzheimer’s patients. While not dismissing the role of these factors, the aforementioned theory that has resurfaced, labeled ‘the pathogen hypothesis’, says that microbial infections are causing the tau tangles and buildup of amyloid proteins, resulting in the ensuing cell death. According to Dr. Brian Balin, Director of the Center for Chronic Disorders of Aging at Philadelphia College of Osteopathic Medicine and co-author of the editorial in the Journal of Alzheimer’s Disease, amyloid proteins play a part in the disease, but only in response to the initial inflammation caused by the microbial infection that is attacking the brain.

Senior Woman Memory Loss

Earlier Examinations of the Pathogen Theory Were Not Conclusive

The pathogen theory is not new. In 1979, a study was published in The Lancet, which reported that scientists at the University of Manchester examined patients carrying APOE є4 whose brains were infected with HSV-1. They found that the prevalence of Alzheimer’s was 12 times higher than when only the gene was present or when there was an infection. A 2010 study at Harvard University, headed by Dr. Rudolph Tanzi, Director of Massachusetts Hospital’s Genetics and Aging Research Center, found that amyloid protein seems to accumulate in response to infection. In research conducted since 2010, Dr. Tanzi has found that amyloid protein increases as a defense mechanism to protect the brain from the infection. One of the points of opposition, though, is that HSV-1 can also be found in the brains of healthy older people.

There Are Major Ramifications If the Theory Can Be Proven

If conclusive evidence can be found that microbial infections are a causative agent in the onset of Alzheimer’s disease, it would dramatically alter the way we approach the disease. Instead of dealing with the consequences, patients could be given a vaccine against the infections.

How to Prove the Theory?

The major stumbling block to proving the theory is that it is not possible to determine if infections such as HSV-1 are present in the brain as long as the patient is still living. Only upon death and autopsy can the brain be examined for these microbial infections. It will require many more years of clinical trials to determine if the pathogen theory is valid. Nevertheless, researchers such as Dr. Balin and others believe it is more than worth it to continue with the research. They hope the upcoming editorial will give credence to their approach and also free up much needed funding.