Archives for December 2014

Be Wise…Immunize!

(Family Caregiver Alliance) Protect your loved ones. Talk to your doctor about immunization against the flu and pneumonia.


The following Fact Sheet is available as a free download in PDF format. To view and print this file you will need Adobe Acrobat Reader. It is available as a free download by clicking here.

Be Wise…Immunize! (English)

Sea prudente… ¡Vacúnese! (Spanish)

當個聰明人,接受免疫注射! (Chinese Traditional)

Будьте мудрымиделайте прививки (Russian)

Chích Ngöøa laø Khoân Ngoan! (Vietnamese)


©Family Caregiver Alliance


Why Do So Many People with Alzheimer’s Disease Appear to be Seeing Things Incorrectly?

(Alzheimer’s Society) Alzheimer’s disease (AD) is often (but mistakenly) defined as simply a memory or cognitive disorder, but the true picture is more complicated.

Alzheimer’s disease is more accurately described as a visual-perceptual-cognitive disorder. Failing to understand the complexities of the illness can lead to many misunderstandings about the difficulties that people with dementia can face.

Looking but Not Seeing

Seeing and perceiving is more than just taking in images in focus. Vision is seeing with the eyes. Perceiving is making sense of what eyes and the other senses are receiving. It requires the ability to co-ordinate all the components of the visual system with the brain’s ability to process that information. It is a complex process, and requires the co-ordination of every aspect of our ability to manage and make sense of information.

Revising the Expectation that ‘Hallucinations are Frequent in Alzheimer’s Disease’

Hallucinations are where people see something although there is no stimulus to see it.  This is not the same as seeing something inaccurately- in a distorted, unclear way, or not recognising what is being seen, or, not being able to ‘problem solve’ that something is a visual illusion.  When there is damage to the visual system, people with dementia may not know they are seeing inaccurately. Also, limitations in language ability may make descriptions of what they’ve seen unclear to listeners.

Hallucinations in people with Alzheimer’s disease are reported at between 13 and 73 per cent, with an average of 40 per cent. This suggests they are a common, and even expected, occurrence. Two studies looking at case notes have found that many events classified by GPs as ‘hallucinations’ were actually more accurately categorised as illusions, misperceptions, misidentifications or naming errors. The studies found that only about 3 per cent of people with AD had “possible visual hallucinations”.

Visual and other types of sensory hallucinations were found more frequently in groups of people with other sorts of dementia and illness- especially those with infections.

Why Do So Many People with Alzheimer’s Disease Appear to be Seeing Things Incorrectly?

We need to take into consideration several factors:

  • Normal deterioration in sight due to ageing.
  • The possibility of illness affecting vision – such as cataracts, glaucoma, macular degeneration.
  • Damage to the visual system as part of the damage to the brain caused by Alzheimer’s disease.
  • The interaction between mistakes in seeing and mistakes in thinking.

Mistakes in Seeing and Thinking

People with Alzheimer’s disease appear to experience a combination of ‘visual mistakes’ and ‘thinking mistakes’, leading to a combined ‘visuo-perceptual-cognitive’ illness.

Some of the errors commonly made include:

  • Mistaking reflections in shiny surfaces and mirrors.
  • Misinterpretting patterns (and water and dirt marks).
  • Anxiety about stepping over carpet rods, thinking they signify a change of level.
  • Refusing to get into an empty lift if it appears full of people because of their own reflection (s) in multiple mirrors.
  • Commenting on ‘little people in the corner of the room’ (people on television).

Minimizing Visual-perceptual Problems

The single biggest thing that can help vision is to improve lighting levels. Better lighting can also help prevent falls, and has also been reported to reduce genuine visual hallucinations.


All content © 2014 Alzheimer’s Society.


The Dementia That Is Not Alzheimer’s Disease

(Science Daily) Lewy body dementia (LBD) — a complex, challenging and surprisingly common brain disease — is often misdiagnosed as its “cousin,” Alzheimer’s disease. And that could lead to devastating results.

According to the Lewy Body Dementia Association (LBDA), accurate and early diagnosis is critical because people with LBD typically have sensitivities to medication, and many drugs prescribed for Alzheimer’s can be very harmful to those with LBD.

Although, LBD is the second most common cause of progressive dementia it is not well recognized by physicians, especially primary care and general health care providers.

“While the symptoms of LBD may be similar to Alzheimer’s and Parkinson’s disease, the treatment strategy is more challenging because fewer medications can be used safely,” warns Howard I. Hurtig, M.D., Chair, Department of Neurology, Pennsylvania Hospital, and member of the LBDA Scientific Advisory Council.

“I cannot overemphasize the need to avoid medications that can worsen the symptoms of LBD. Every patient with this disease and their caregivers should be familiar with the list of acceptable and forbidden drugs.”

Is it Alzheimer’s or LBD?

These two diseases share some clinical and biological similarities that can make them difficult for many physicians to distinguish. Dementia experts are more experienced at differentiating between dementia types.

Alzheimer’s disease affects cognitive function, including making new experiences into memories. The disorder in LBD affects different aspects of cognition, such as problem solving and complex reasoning and movement.

LBDA has just issued a new brochure — Lewy Who? Recognizing when it’s not Parkinson’s or Alzheimer’s Disease — that offers a symptom comparison chart that can help clarify the confusion. It can be downloaded from the website.

A Different Diagnosis

Lewy body dementia, which affects 1.4 million Americans, refers to two related diagnoses: dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD). Both DLB and PDD are considered Lewy body dementias.

With DLB, cognitive (thinking) symptoms appear before Parkinson-like movement problems. With PDD, disabling cognitive symptoms do not develop until more than a year after movement problems begin.

LBD is characterized by an abnormal build up of Lewy bodies (alpha-synuclein protein deposits) in the areas of the brain that regulate behavior, memory, movement and personality. The most prominent symptoms of Parkinson’s disease affect motor abilities. Alzheimer’s disease primarily affects areas of the brain involving learning and memory. A specialist like a neurologist, geriatric psychiatrist or a neuropsychologist may be needed to distinguish the symptoms and provide an accurate diagnosis.


The above story is based on materials provided by Lewy Body Dementia Association. Note: Materials may be edited for content and length.

Lewy Body Dementia Association. (2014, December 19). The dementia that is not Alzheimer’s disease. ScienceDaily. Retrieved December 28, 2014 from

Copyright 2014 by ScienceDaily, LLC or by third-party sources, where indicated.


New Research Suggests an Existing Drug, Riluzole, May Prevent Foggy ‘Old Age’ Brain

(Rockefeller University) Forgetfulness, it turns out, is all in the head. Scientists have shown that fading memory and clouding judgment, the type that comes with advancing age, show up as lost and altered connections between neurons in the brain. But new experiments suggest an existing drug, known as riluzole and already on the market as a treatment for ALS, may help prevent these changes.

141219_mcewenBetter memory makers: When researchers looked at certain neurons (similar to the one shown on top) in rats treated with riluzole, they found an important change in one brain region, the hippocampus: more clusters of so-called spines, receiving connections that extend from the branches of a neuron (bottom).

Researchers at The Rockefeller University and The Icahn School of Medicine at Mount Sinai found they could stop normal, age-related memory loss in rats by treating them with riluzole. This treatment, they found, prompted changes known to improve connections, and as a result, communication, between certain neurons within the brain’s hippocampus.

“By examining the neurological changes that occurred after riluzole treatment, we discovered one way in which the brain’s ability to reorganize itself — its neuroplasticity — can be marshaled to protect it against some of the deterioration that can accompany old age, at least in rodents,”

says co-senior study author Alfred E. Mirsky Professor Bruce McEwen, head of the Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology. The research is published this week in Proceedings of the National Academy of Sciences.

Neurons connect to one another to form circuits connecting certain parts of the brain, and they communicate using a chemical signal known as glutamate. But too much glutamate can cause damage; excess can spill out and excite connecting neurons in the wrong spot. In the case of age-related cognitive decline, this process damages neurons at the points where they connect — their synapses. In neurodegenerative disorders, such as Alzheimer’s disease, this contributes to the death of neurons.

Used to slow the progress of another neurodegenerative condition, ALS (also known as Lou Gehrig’s disease), riluzole was an obvious choice as a potential treatment, because it works by helping to control glutamate release and uptake, preventing harmful spillover. The researchers began giving riluzole to rats once they reached 10 months old, the rat equivalent of middle age, when their cognitive decline typically begins.

After 17 weeks of treatment, the researchers tested the rats’ spatial memory — the type of memory most readily studied in animals — and found they performed better than their untreated peers, and almost as well as young rats. For instance, when placed in a maze they had already explored, the treated rats recognized an unfamiliar arm as such and spent more time investigating it.

When the researchers looked inside the brains of riluzole-treated rats, they found telling changes to the vulnerable glutamate sensing circuitry within the hippocampus, a brain region implicated in memory and emotion.

“We have found that in many cases, aging involves synaptic changes that decrease synaptic strength, the plasticity of synapses, or both,” said John Morrison, professor of neuroscience and the Friedman Brain Institute and dean of basic sciences and the Graduate School of Biomedical Sciences at Mount Sinai.

“The fact that riluzole increased the clustering of only the thin, most plastic spines, suggests that its enhancement of memory results from both an increase in synaptic strength and synaptic plasticity, which might explain its therapeutic effectiveness.”

In this case, the clusters involved thin spines, a rapidly adaptable type of spine. The riluzole-treated animals had more clustering than the young animals and their untreated peers, who had the least. This discovery led the researchers to speculate that, in general, the aged brain may compensate by increasing clustering. Riluzole appears to enhance this mechanism.

Taking advantage of the overlap of neural circuits vulnerable to age-related cognitive decline and Alzheimer’s disease, Pereira is currently conducting a clinical trial to test the effectiveness of riluzole for patients with mild Alzheimer’s.


Copyright © 2004–2014 The Rockefeller University. All rights reserved.


Memory Loss Associated with Alzheimer’s Reversed: Small Trial Succeeds Using Systems Approach to Memory Disorders

(University of California, Los Angeles, Health Sciences) Patient one had two years of progressive memory loss. She was considering quitting her job, which involved analyzing data and writing reports, she got disoriented driving, and mixed up the names of her pets. Patient two kept forgetting once familiar faces at work, forgot his gym locker combination, and had to have his assistants constantly remind him of his work schedule. Patient three’s memory was so bad she used an iPad to record everything, then forgot her password. Her children noticed she commonly lost her train of thought in mid-sentence, and often asked them if they had carried out the tasks that she mistakenly thought she had asked them to do.

Since its first description over 100 years ago, Alzheimer’s disease has been without effective treatment. That may finally be about to change: in the first, small study of a novel, personalized and comprehensive program to reverse memory loss, nine of 10 participants, including the ones above, displayed subjective or objective improvement in their memories beginning within three to six months after the program’s start.

Of the six patients who had to discontinue working or were struggling with their jobs at the time they joined the study, all were able to return to work or continue working with improved performance. Improvements have been sustained, and as of this writing the longest patient follow-up is two and one-half years from initial treatment.

These first ten included patients with memory loss associated with Alzheimer’s disease (AD), amnestic mild cognitive impairment (aMCI), or subjective cognitive impairment (SCI; when a patient reports cognitive problems). One patient, diagnosed with late stage Alzheimer’s, did not improve.

The study, which comes jointly from the UCLA Mary S. Easton Center for Alzheimer’s Disease Research and the Buck Institute for Research on Aging, is the first to suggest that memory loss in patients may be reversed, and improvement sustained, using a complex, 36-point therapeutic program that involves comprehensive changes in diet, brain stimulation, exercise, optimization of sleep, specific pharmaceuticals and vitamins, and multiple additional steps that affect brain chemistry.

The findings, published in the current online edition of the journal Aging, “are very encouraging. However, at the current time the results are anecdotal, and therefore a more extensive, controlled clinical trial is warranted,” said Dale Bredesen, the Augustus Rose Professor of Neurology and Director of the Easton Center at UCLA, a professor at the Buck Institute, and the author of the paper.

In the case of Alzheimer’s disease, Bredesen notes, there is not one drug that has been developed that stops or even slows the disease’s progression, and drugs have only had modest effects on symptoms.

“In the past decade alone, hundreds of clinical trials have been conducted for Alzheimer’s at an aggregate cost of over a billion dollars, without success,” he said.

Other chronic illnesses such as cardiovascular disease, cancer, and HIV, have been improved through the use of combination therapies, he noted. Yet in the case of Alzheimer’s and other memory disorders, comprehensive combination therapies have not been explored. Yet over the past few decades, genetic and biochemical research has revealed an extensive network of molecular interactions involved in AD pathogenesis.

“That suggested that a broader-based therapeutics approach, rather than a single drug that aims at a single target, may be feasible and potentially more effective for the treatment of cognitive decline due to Alzheimer’s,” said Bredesen.

While extensive preclinical studies from numerous laboratories have identified single pathogenetic targets for potential intervention, in human studies, such single target therapeutic approaches have not borne out. But, said Bredesen, it’s possible addressing multiple targets within the network underlying AD may be successful even when each target is affected in a relatively modest way.

“In other words,” he said, “the effects of the various targets may be additive, or even synergistic.”

The uniform failure of drug trials in Alzheimer’s influenced Bredesen’s research to get a better understanding of the fundamental nature of the disease. His laboratory has found evidence that Alzheimer’s disease stems from an imbalance in nerve cell signaling: in the normal brain, specific signals foster nerve connections and memory making, while balancing signals support memory loss, allowing irrelevant information to be forgotten. But in Alzheimer’s disease, the balance of these opposing signals is disturbed, nerve connections are suppressed, and memories are lost.

The model of multiple targets and an imbalance in signaling runs contrary to the popular dogma that Alzheimer’s is a disease of toxicity, caused by the accumulation of sticky plaques in the brain. Bredesen believes the amyloid beta peptide, the source of the plaques, has a normal function in the brain — as part of a larger set of molecules that promotes signals that cause nerve connections to lapse. Thus the increase in the peptide that occurs in Alzheimer’s disease shifts the memory-making vs. memory-breaking balance in favor of memory loss.

Given all this, Bredesen thought that rather than a single targeted agent, the solution might be a systems type approach, the kind that is in line with the approach taken with other chronic illnesses — a multiple-component system.

“The existing Alzheimer’s drugs affect a single target, but Alzheimer’s disease is more complex. Imagine having a roof with 36 holes in it, and your drug patched one hole very well — the drug may have worked, a single “hole” may have been fixed, but you still have 35 other leaks, and so the underlying process may not be affected much.”

Bredesen’s approach is personalized to the patient, based on extensive testing to determine what is affecting the plasticity signaling network of the brain. As one example, in the case of the patient with the demanding job who was forgetting her way home, her therapeutic program consisted of some, but not all of the components involved with Bredesen’s therapeutic program, and included:

(1) eliminating all simple carbohydrates, leading to a weight loss of 20 pounds;

(2) eliminating gluten and processed food from her diet, with increased vegetables, fruits, and non-farmed fish;

(3) to reduce stress, she began yoga;

(4) as a second measure to reduce the stress of her job, she began to meditate for 20 minutes twice per day;

(5) she took melatonin each night;

(6) she increased her sleep from 4-5 hours per night to 7-8 hours per night;

(7) she took methylcobalamin each day;

(8) she took vitamin D3 each day;

(9) fish oil each day;

(10) CoQ10 each day;

(11) she optimized her oral hygiene using an electric flosser and electric toothbrush;

(12) following discussion with her primary care provider, she reinstated hormone replacement therapy that had been discontinued;

(13) she fasted for a minimum of 12 hours between dinner and breakfast, and for a minimum of three hours between dinner and bedtime;

(14) she exercised for a minimum of 30 minutes, 4-6 days per week.

The results for nine of the 10 patients reported in the paper suggest that memory loss may be reversed, and improvement sustained with this therapeutic program, said Bredesen.

“This is the first successful demonstration,” he noted, but he cautioned that the results are anecdotal, and therefore a more extensive, controlled clinical trial is needed.

The downside to this program is its complexity. It is not easy to follow, with the burden falling on the patients and caregivers, and none of the patients were able to stick to the entire protocol. The significant diet and lifestyle changes, and multiple pills required each day, were the two most common complaints. The good news, though, said Bredesen, are the side effects:

“It is noteworthy that the major side effect of this therapeutic system is improved health and an optimal body mass index, a stark contrast to the side effects of many drugs.”

The results for nine of the 10 patients reported in the paper suggest that memory loss may be reversed, and improvement sustained with this therapeutic program, said Bredesen.

“This is the first successful demonstration,” he noted, but he cautioned that the results need to be replicated. “The current, anecdotal results require a larger trial, not only to confirm or refute the results reported here, but also to address key questions raised, such as the degree of improvement that can be achieved routinely, how late in the course of cognitive decline reversal can be effected, whether such an approach may be effective in patients with familial Alzheimer’s disease, and last, how long improvement can be sustained,” he said.

Cognitive decline is a major concern of the aging population. Already, Alzheimer’s disease affects approximately 5.4 million Americans and 30 million people globally. Without effective prevention and treatment, the prospects for the future are bleak. By 2050, it’s estimated that 160 million people globally will have the disease, including 13 million Americans, leading to potential bankruptcy of the Medicare system. Unlike several other chronic illnesses, Alzheimer’s disease is on the rise–recent estimates suggest that AD has become the third leading cause of death in the United States behind cardiovascular disease and cancer.


Story Source:

The above story is based on materials provided by University of California, Los Angeles (UCLA), Health Sciences. Note: Materials may be edited for content and length.

Journal Reference:

Dale E. Bredesen. Reversal of cognitive decline: A novel therapeutic program. Aging, September 2014

University of California, Los Angeles (UCLA), Health Sciences. (2014, September 30). Memory loss associated with Alzheimer’s reversed: Small trial succeeds using systems approach to memory disorders. ScienceDaily. Retrieved October 1, 2014 from

Copyright 2014 by ScienceDaily, LLC or by third-party sources, where indicated.


Target Risk Factors for Dementia Prevention

Int J Geriatr Psychiatry. 2014 Dec 12. doi: 10.1002/gps.4245. [Epub ahead of print]

Target risk factors for dementia prevention: a systematic review and Delphi consensus study on the evidence from observational studies.

Deckers K1, van Boxtel MP, Schiepers OJ, de Vugt M, Muñoz Sánchez JL, Anstey KJ, Brayne C, Dartigues JF, Engedal K, Kivipelto M, Ritchie K, Starr JM, Yaffe K, Irving K, Verhey FR, Köhler S.



Dementia has a multifactorial etiology, but the importance of individual health and lifestyle related risk factors is often uncertain or based on few studies. The goal of this paper is to identify the major modifiable risk factors for dementia as a first step in developing an effective preventive strategy and promoting healthy late life cognitive functioning.


A mixed-method approach combined findings from a systematic literature review and a Delphi consensus study. The literature search was conducted in PubMed and updated an earlier review by the United States National Institutes of Health from 2010. We reviewed the available evidence from observational epidemiological studies. The online Delphi study asked eight international experts to rank and weigh each risk factor for its importance for dementia prevention.


Out of 3127 abstracts, 291 were included in the review. There was good agreement between modifiable risk factors identified in the literature review and risk factors named spontaneously by experts. After triangulation of both methods and re-weighting by experts, strongest support was found for depression, (midlife) hypertension, physical inactivity, diabetes, (midlife) obesity, hyperlipidemia, and smoking, while more research is needed for coronary heart disease, renal dysfunction, diet, and cognitive activity.


Findings provide good support for several somatic and lifestyle factors and will be used to inform the design of a new multicenter trial into dementia prevention.


Copyright © 2014 John Wiley & Sons, Ltd.


Use of Dextromethorphan in Adults with Neurological Damage Conditions

Drugs. 2014 Nov 25. [Epub ahead of print]

Dextromethorphan/Quinidine: A Review of Its Use in Adults with Pseudobulbar Affect.

Yang LP1, Deeks ED.


Fixed-dose dextromethorphan/quinidine capsules (Nuedexta®) utilize quinidine to inhibit the metabolism of dextromethorphan, enabling high plasma dextromethorphan concentrations to be reached without using a larger dose of the drug.

The drug combination is the first treatment to be approved for pseudobulbar affect (PBA), a condition of contextually inappropriate/exaggerated emotional expression that often occurs in adults with neurological damage conditions, such as amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), stroke, traumatic brain injury, Alzheimer’s disease or Parkinson’s disease.

Dextromethorphan/quinidine at the recommended dosages of 20/10 or 30/10 mg twice daily reduced the rate of PBA episodes and improved PBA severity in a 12-week, double-blind, placebo-controlled trial in adults with ALS or MS (STAR), with further improvements in the severity of the condition observed in a 12-week open-label extension phase.

Dextromethorphan/quinidine 20/10 mg twice daily also improved PBA secondary to dementia in a cohort of a 12-week noncomparative trial (PRISM II). The drug combination was generally well tolerated in these studies, with no particular safety or tolerability concerns. Although longer-term efficacy and tolerability data for dextromethorphan/quinidine 20/10 or 30/10 mg twice daily would be beneficial, current evidence indicates that it is a useful option in the treatment of adults with PBA.



Scientists Locate ‘Homing Signal’ in the Brain, Explaining Why Some People are Better Navigators

(University of London) The part of the brain that tells us the direction to travel when we navigate has been identified by UCL scientists, and the strength of its signal predicts how well people can navigate.

Homing signal in the brain

It has long been known that some people are better at navigating than others, but until now it has been unclear why. The latest study, funded by the Wellcome Trust and published in Current Biology, shows that the strength and reliability of ‘homing signals’ in the human brain vary among people and can predict navigational ability.

In order to successfully navigate to a destination, you need to know which direction you are currently facing and which direction to travel in. For example, ‘I am facing north and want to head east’. It is already known that mammals have brain cells that signal the direction that they are currently facing, a discovery that formed part of the 2014 Nobel Prize in Physiology or Medicine to UCL Professor John O’Keefe.

The latest research reveals that the part of the brain that signals which direction you are facing, called the entorhinal region, is also used to signal the direction in which you need to travel to reach your destination.

This part of the brain tells you not only which direction you are currently facing, but also which direction you should be facing in the future. In other words, the researchers have found where our ‘sense of direction’ comes from in the brain and worked out a way to measure it using functional magnetic resonance imaging (fMRI).

“This type of ‘homing signal’ has been thought to exist for many years, but until now it has remained purely speculation,” explains Dr Hugo Spiers (UCL Experimental Psychology), who led the study.”

“Studies on London cab drivers have shown that the first thing they do when they work out a route is calculate which direction they need to head in. We now know that the entorhinal cortex is responsible for such calculations and the quality of signals from this region seem to determine how good someone’s navigational skills will be.”

In the study, 16 healthy volunteers were asked to navigate a simple square environment simulated on a computer. Each wall had a picture of a different landscape, and each corner contained a different object. Participants were placed in a corner of the environment, facing a certain direction and asked how to navigate to an object in another corner.

“In this simple test, we were looking to see which areas of the brain were active when participants were considering different directions,” says Dr Spiers.

“We were surprised to see that the strength and consistency of brain signals from the entorhinal region noticeably influenced people’s performance in such a basic task. We now need to investigate the effect in more complex navigational tasks, but I would expect the differences in entorhinal activity to have a larger impact on more complex tasks.”

Dr Martin Chadwick (UCL Experimental Psychology), lead author of the study, said:

“Our results provide evidence to support the idea that your internal ‘compass’ readjusts as you move through the environment. For example, if you turn left then your entorhinal region should process this to shift your facing direction and goal direction accordingly. If you get lost after taking too many turns, this may be because your brain could not keep up and failed to adjust your facing and goal directions.”

The entorhinal region is one of the first parts of the brain affected by Alzheimer’s disease, so the findings may also help to explain why people start to get lost in the early stages of the disease. The researchers hope to develop their simple simulation task so that it might be used to aid early diagnosis and monitor the progression of the disease.

Dr John Isaac, Head of Neuroscience and Mental Health at the Wellcome Trust said:

“Neuroscientists have made huge advances in our understanding of how we navigate space, widely recognised after this year’s Nobel Prizes, and this research is yet another step forward.

Why some people are better navigators than others is intrinsically interesting, but it also helps us explain the processes that go wrong in people with degenerative brain disorders such as dementia.

An estimated 850,000 people are living with dementia in the UK, many of whom suffer deterioration in their navigational skills, leaving them lost and confused.”


© UCL 1999–2014