Age-Related Dementia May Begin With Neurons' Inability to Rid Themselves of Unwanted Proteins

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Science Daily

 

A team of European scientists from the University Medical Center Hamburg-Eppendorf (UKE) and the Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) at the University of Cologne in Germany has taken an important step closer to understanding the root cause of age-related dementia. In research involving both worms and mice, they have found that age-related dementia is likely the result of a declining ability of neurons to dispose of unwanted aggregated proteins.

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As protein disposal becomes significantly less efficient with increasing age, the buildup of these unwanted proteins ultimately leads to the development and progression of dementia.

"By studying disease progression in dementia, specifically by focusing on mechanisms neurons use to dispose of unwanted proteins, we show how these are interconnected and how these mechanisms deteriorate over time," said Markus Glatzel, M.D., a researcher involved in the work from the Institute of Neuropathology at UKE in Hamburg, Germany. "This gives us a better understanding as to why dementias affect older persons; the ultimate aim is to use these insights to devise novel therapies to restore the full capacity of protein disposal in aged neurons."
To make this discovery, scientists carried out their experiments in both worm and mouse models that had a genetically-determined dementia in which the disease was caused by protein accumulation in neurons. In the worm model, researchers in the lab of Thorsten Hoppe, Ph.D., from the CECAD Cluster of Excellence could inactivate distinct routes used for the disposal of the unwanted proteins. Results provided valuable insight into the mechanisms that neurons use to cope with protein accumulation. These pathways were then assessed in young and aged mice. This study provides an explanation of why dementias exponentially increase with age. Additionally, neuron protein disposal methods may offer a therapeutic target for the development of drugs to treat and/or prevent dementias.
"This is an exciting study that helps us understand what's going wrong at a cellular level in age-related dementias," said Mark Johnston, Ph.D., Editor-in-Chief of the journal GENETICS. "This research holds possibilities for future identification of substances that can prevent, stop, or reverse this cellular malfunction in humans."

Misplaced molecules: new insights into the causes of dementia

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

HealthCanal

Munich, March - A team of German and Belgian researchers has succeeded in gaining new insights into the causes of certain movement disorders and forms of dementia. Scientists including Bettina Schmid and Christian Haass from the German Center for Neurodegenerative Diseases (DZNE) in Munich and the Ludwig-Maximilians-Universität (LMU) were able to reproduce disease symptoms typical of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) in zebrafish. A shortage of a protein called TDP-43 caused muscle wasting and stunted nerve cells. This finding supports the idea that malfunction of this protein plays a decisive role in ALS and FTD. The study is published in the “Proceedings of the National Academy of Sciences of the USA” (PNAS).

ALS is an incurable neurological disease which manifests as rapidly progressing muscle wasting. Both limbs and respiratory muscles are affected. This leads to impaired mobility and breathing problems. Patients commonly die within a few years after the symptoms emerged. In rare cases, of which the British physicist Stephen Hawking is the most notable, patients can live with the disease for a long time. In Germany estimates show over 150,000 patients suffering from ALS – an average of 1 in 500 people.

 

Research illuminates why stimulating environment may protect against Alzheimer's disease

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

Medical News

 

"Use it or lose it." The saying could apply especially to the brain when it comes to protecting against Alzheimer's disease. Previous studies have shown that keeping the mind active, exercising and social interactions may help delay the onset of dementia in Alzheimer's disease.

Now, a new study led by Dennis Selkoe, MD, co-director of the Center for Neurologic Diseases in the BWH Department of Neurology, provides specific pre-clinical scientific evidence supporting the concept that prolonged and intensive stimulation by an enriched environment, especially regular exposure to new activities, may have beneficial effects in delaying one of the key negative factors in Alzheimer's disease.
The study will be published online on March 6, 2013 in Neuron.
Alzheimer's disease occurs when a protein called amyloid beta accumulates and forms "senile plaques" in the brain. This protein accumulation can block nerve cells in the brain from properly communicating with one another. This may gradually lead to an erosion of a person's mental processes, such as memory, attention, and the ability to learn, understand and process information.
The BWH researchers used a wild-type mouse model when evaluating how the environment might affect Alzheimer's disease. Unlike other pre-clinical models used in Alzheimer's disease research, wild-type mice tend to more closely mimic the scenario of average humans developing the disease under normal environmental conditions, rather than being strongly genetically pre-disposed to the disease.
Selkoe and his team found that prolonged exposure to an enriched environment activated certain adrenalin-related brain receptors which triggered a signaling pathway that prevented amyloid beta protein from weakening the communication between nerve cells in the brain's "memory center," the hippocampus. The hippocampus plays an important role in both short- and long-term memory.
The ability of an enriched, novel environment to prevent amyloid beta protein from affecting the signaling strength and communication between nerve cells was seen in both young and middle-aged wild-type mice.

"This part of our work suggests that prolonged exposure to a richer, more novel environment beginning even in middle age might help protect the hippocampus from the bad effects of amyloid beta, which builds up to toxic levels in one hundred percent of Alzheimer patients," said Selkoe. Moreover, the scientists found that exposing the brain to novel activities in particular provided greater protection against Alzheimer's disease than did just aerobic exercise. According to the researchers, this observation may be due to stimulation that occurred not only physically, but also mentally, when the mice moved quickly from one novel object to another.
"This work helps provide a molecular mechanism for why a richer environment can help lessen the memory-eroding effects of the build-up of amyloid beta protein with age," said Selkoe. "They point to basic scientific reasons for the apparent lessening of AD risk in people with cognitively richer and more complex experiences during life."
Source: Brigham and Women's Hospital

5 foods to prevent dementia

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

By Vicky Hallett, The Washington Post

Metro Creative

We love our hearts. But what are our brains — chopped liver? Neal Barnard, an adjunct associate professor of medicine at the George Washington University School of Medicine and Health Sciences, says how we eat can improve not just the function of our tickers, but also the longevity of our noggins.
In his new book, “Power Foods for the Brain” ($27), and his PBS special, “Protect Your Memory” (debuting on public television on Saturday; check local listings), he outlines his nutrition plan to stave off Alzheimer’s and dementia. Barnard took us shopping to point out some smart choices. And, no, chopped liver wasn’t one of them.
— Walnuts: Vitamin E can be a brain booster, Barnard says, noting a Dutch study that showed that people with the most vitamin E in their diets cut their risk of Alzheimer’s by 25 percent. The best sources are nuts and seeds. Barnard generally opts for walnuts, which he enjoys shaved over a salad. (That also helps him limit his intake so he doesn’t overdo it with calories.)
— Blueberries: “None of these have any cholesterol,” he says, waving at the produce display. And that’s important for the brain because clogged-up arteries translate into reduced mental function. But he’s particularly fond of this antioxidant-rich fruit that’s been shown (in a small study) to help people with memory problems.
— Broccoli: Folate sounds like foliage, which is what it is, Barnard says. And in combination with vitamins B6 and B12 (which he recommends taking supplements of), it can eliminate homocysteine — a destructive molecule that messes with the heart and brain.
— Sweet Potatoes: Wondering how to get your B6? Throw some of these root veggies into your basket. (Bananas are another good source.) Barnard says they’re a staple in the diet in Okinawa, a place where people have been found to have exceptional brain function in old age.
— Wine: Too much vino can mess with memory, obviously. But a glass or two a night has been shown to cut Alzheimer’s risk significantly. In theory, red wine is the better choice, Barnard says, because the resveratrol it contains may be good for your heart. But when it comes to the brain, a glass of any alcohol appears to offer similar protection.

Drug Shows Potential to Delay Onset or Progression of Alzheimer's Disease

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

Science Daily

A research team led by Robert Nagele, PhD, of the New Jersey Institute for Successful Aging (NJISA) at the University of Medicine and Dentistry of New Jersey (UMDNJ)-School of Osteopathic Medicine, has demonstrated that the anti-atherosclerosis drug darapladib can significantly reduce leaks in the blood brain barrier. This finding potentially opens the door to new therapies to prevent the onset or the progression of Alzheimer's disease.

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Writing in the Journal of Alzheimer's Disease (currently in press), the researchers describe findings involving the use of darapladib in animal models that had been induced to develop diabetes mellitus and hypercholesterolemia (DMHC), which are considered to be major risk factors for Alzheimer's disease.
"Diabetes and hypercholesterolemia are associated with an increased permeability of the blood-brain barrier, and it is becoming increasingly clear that this blood-brain barrier breakdown contributes to neurodegenerative diseases such as Alzheimer's," Nagele said. "Darapladib appears to be able to reduce this permeability to levels comparable to those found in normal, non-DMHC controls, and suggests a link between this permeability and the deposition of amyloid peptides in the brain."
The study involved 28 animal (pig) models that were divided into three groups -- DMHC animals treated with a 10 mg/day dose of darapladib; DMHC animals that received no treatment; and non-DMHC controls. Post-mortem analysis of the brains of the darapladib-treated animals showed significant decreases in blood-brain barrier leakage and in the density of amyloid-positive neurons in the cerebral cortices. Interestingly, the amyloid peptides that leaked into the brain tissue were found almost exclusively in the pyramidal neurons of the cerebral cortex, one of the earliest pathologies of the development of Alzheimer's disease.
"Because our results suggest that these metabolic disorders can trigger neurodegenerative changes through blood-brain barrier compromise, therapies -- such as darapladib -- that can reduce vascular leaks have great potential for delaying the onset or slowing the progression of diseases like Alzheimer's," said the study's lead author, Nimish Acharya, PhD, of the NJISA and the UMDNJ-Graduate School of Biomedical Sciences. "The clinical, caregiving and financial impact of such an effect cannot be overestimated."
This study was supported by funding from GlaxoSmithKline through an industry-academic alliance via the Alternative Drug Discovery Initiative with the University of Pennsylvania School of Medicine.

Will this drug work for those with dementia

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

Inquisitr

 

new Alzheimer’s Disease (AD) drug may have been found on the pharmacy shelves, where it’s currently FDA-approved as a treatment for a different disease. That’s the conclusion of a National Institutes of Health funded study of Buphenyl on mice, according to a recent report by Rush University Medical Center researchers published in the Journal of Biological Chemistry.
Kalipada Pahan, a neurologist who was also the lead investigator, said that they were looking into a family of proteins that vanish in the brains of patients with AD. The proteins are called neurotrophic factors, and they simply help brain cells work and survive. As the proteins disappear from the victim’s brain, the patient loses the ability to learn and remember.

 

If doctors had a simple pill that replaced these proteins, it might be a fast, cost effective way to help people with the disease. Pahan’s study showed that when they fed the drug to mice, it was digested in a way that allowed it to go to the brain and increase the number of the helpful proteins found there

The race is on to find a cure or at least an effective treatment to slow the progression of AD. Because of the aging worldwide population, the number of people suffering from Alzheimer’s disease is projected to triple by 2050. Research has suggested that people try everything from drinking green tea to asking your doctor about a prescription for beta blockers.

Buphenyl may have an important advantage for elders who need help now. Although new to Alzheimer’s patients, it’s already on the market. It’s currently prescribed to treat hyperammonemia, a life-threatening disease that allows high levels of ammonia to build up in the bloodstream.
Of course, testing Buphenyl on mouse brains is only the first step. Next, the researchers want to test the new drug on actual Alzheimer’s patients.

Good mood can improve elderly cognition

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Scope-Stanford University

 

Past research has shown that developing a positive outlook on the aging process can have a significant effect on a person’s overall health, happiness and longevity. Now findings published in the latest issue of Cognition and Emotion suggest that being in a good mood can help boost decision making and working memory in older adults.

In the study (subscription required), which involved individuals age 63 to 85, researchers put half of the participants in a better mood by giving them thank-you cards and bags of candy tied when they arrived for the experiments. Those in the “neutral mood” group did not receive a card or candy.

 
Participants completed two experiments. The first tested decision making. Individuals were given three dollars in quarters, instructed to play a computer card game and told to win as much money as they could. A follow-up experiment gauged participants’ working memory. Researchers fed the participants increasingly long series of letters and numbers and asked participants to state them in increasing numeric and alphabetic order. Science Daily reports:

The findings were clear: older adults who were put into a good mood chose significantly better than those who were in the neutral mood.
These results are significant because this decision-making task was experiential, meaning that the participants knew nothing about the card values at the beginning of the experiment and had to learn through trial and error.
…
Results showed that the older adults who were induced into a good mood scored better on this test of working memory.
…
A positive mood did not help these older adults on some cognitive measures, such as speed of processing or vocabulary.

The findings are interesting in light of other studies showing that being in a good mood can increase creativity.

Previously: Study shows practicing tai chi may increase brain volume in healthy older adults, Stanford and USC study shows soy supplements may have no significant effect on cognitive function, More research suggests brain exercises boost cognitive function, stave off dementia and The secret to living longer? It’s all in the ‘tude

Age-Related Dementia May Begin With Neurons' Inability to Rid Themselves of Unwanted Proteins

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Here is a great dementia resource for caregivers and healthcare professionals,

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

Science Daily

A team of European scientists from the University Medical Center Hamburg-Eppendorf (UKE) and the Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) at the University of Cologne in Germany has taken an important step closer to understanding the root cause of age-related dementia. In research involving both worms and mice, they have found that age-related dementia is likely the result of a declining ability of neurons to dispose of unwanted aggregated proteins.

---

 

As protein disposal becomes significantly less efficient with increasing age, the buildup of these unwanted proteins ultimately leads to the development and progression of dementia.
"By studying disease progression in dementia, specifically by focusing on mechanisms neurons use to dispose of unwanted proteins, we show how these are interconnected and how these mechanisms deteriorate over time," said Markus Glatzel, M.D., a researcher involved in the work from the Institute of Neuropathology at UKE in Hamburg, Germany. "This gives us a better understanding as to why dementias affect older persons; the ultimate aim is to use these insights to devise novel therapies to restore the full capacity of protein disposal in aged neurons."
To make this discovery, scientists carried out their experiments in both worm and mouse models that had a genetically-determined dementia in which the disease was caused by protein accumulation in neurons. In the worm model, researchers in the lab of Thorsten Hoppe, Ph.D., from the CECAD Cluster of Excellence could inactivate distinct routes used for the disposal of the unwanted proteins. Results provided valuable insight into the mechanisms that neurons use to cope with protein accumulation. These pathways were then assessed in young and aged mice. This study provides an explanation of why dementias exponentially increase with age. Additionally, neuron protein disposal methods may offer a therapeutic target for the development of drugs to treat and/or prevent dementias.
"This is an exciting study that helps us understand what's going wrong at a cellular level in age-related dementias," said Mark Johnston, Ph.D., Editor-in-Chief of the journal GENETICS. "This research holds possibilities for future identification of substances that can prevent, stop, or reverse this cellular malfunction in humans."

Alzheimers is the fastest growing health threat

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

by Maggie Fox, Senior Writer, NBC News

Alzheimer’s disease is the fastest growing threat to health in the United States, but Americans are still most likely to die from diseases caused by their own habits such as overeating and tobacco, according to a new report on global death and disease.

In contrast, AIDS and alcohol are the biggest health threats among Russians, malnutrition threatens children in Africa and Afghanistan and violence is taking the lives of many young men across much of Latin America.
The team at the University of Washington in Seattle looked at thousands of sources of data, from individual death certificates to global surveys on illness, for their report. It compares various causes of death and diseases across 187 countries.
Groups like the Alzheimer’s Association have been warning that the U.S. will have to cope with a tsunami of Alzheimer’s disease as the population ages. A report last month projected that the number of patients with this untreatable form of dementia will triple in the next 40 years, to 13.8 million in 2050.
The University of Washington team looked at Alzheimer's trends and found it’s already up 392 percent as a cause of premature death, as measured by years of life lost. As an overall cause of death – how many people die of Alzheimer's instead of something else – it’s up more than 500 percent.
As for causes of disease, they are mostly self-imposed.
“Overall, the three risk factors that account for the most disease burden in the United States are dietary risks, tobacco smoking, and high body-mass index,” reads the report, called the Global Burden of Diseases, Injuries, and Risk Factors 2010.
Heart disease, lung and throat cancer and stroke cost Americans the most years of life in 2010, the study, led by the university’s Christopher Murray, found. The single biggest risk factor in the U.S. is diet.
But there’s good news. “Of the 25 most important causes of burden, as measured by disability-adjusted life years, interpersonal violence showed the largest decrease, falling by 26 percent from 1990 to 2010,” the report finds
There’s other good news in the report: AIDS infections appear to have peaked globally and people are living longer and healthier lives.
“While HIV/AIDS has exacted a devastating toll on many countries in sub-Saharan Africa, increasing by 328 percent in terms of healthy years lost from 1990 to 2010, the epidemic appears to have peaked in 2004,” the report says.
Death rates from HIV are now falling, according to the World Health Organization. Programs to get people treated with cocktails of lifesaving drugs, which can also prevent new infections, are the reason. “This success is largely attributable to the massive scale-up in antiretroviral therapy over the past decade,” the report reads.
Other rich countries have similar health profiles to the United States. Residents of Britain and Canada both also suffer most from overeating and smoking. In Britain, the single biggest helath risk to children is second-hand smoke.
In contrast, the three biggest causes of poor health in Ecuador are alcohol abuse, poor diet and high blood pressure. Children are the most hurt by poor breastfeeding.
In Afghanistan, most disease is caused by air pollution from household fireplaces and cookstoves, underweight children and poor diet.
“A troubling mortality trend is among young adults, especially young men, who are now dying at very high rates in eastern Europe, central Asia, and eastern and southern Africa. This is largely due to the epidemics of alcohol‐related mortality and HIV/AIDS, respectively,” the report says.
“The average mortality rates among males aged 25 to 39 fell by little more than 19.7 percent over the four decades as compared to much higher declines in other age‐groups.”

INDIVIDUALIZED EATING PROGRAM LOWERS DEPRESSSION IN THOSE WITH DEMENTIA

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Psych Central

Traci Pederson

 

Reviewed by John M. Grohol, Psy.D. Institutionalized dementia patients who received individualized instruction on good eating habits had fewer symptoms of depression six months later, according to a new Taiwanese study published in the Journal of Advanced Nursing.

“The improvement in nutritional status may have led to reduced fatigue and increased vitality,” said the researchers. “Once the participants perceived the improvements in their health, pessimism, the sense of multiple illnesses, hopelessness, or even worthlessness seldom emerged.”

Nutritional status and body mass index increased in patients who received the individualized program, decreased in the control group, and showed little change with the non-individualized program, said the researchers.

Dementia patients often miss out on proper nutrition. As the researchers explained, “identifying foods, transferring foods, chewing, and swallowing” become progressively more difficult for patients with cognitive problems.

Furthermore, previous studies have linked poor nutritional status to depression, in otherwise healthy adults and in those with dementia.

In the current study, the researchers combined Montessori-type methods with a technique called “spaced retrieval.” The goal was to help dementia patients eat more and eat more regularly.

Spaced retrieval is a teaching method that helps people recall information. It involves challenging the person to remember something for increasing time intervals. If it is successfully remembered after 2 minutes, a second challenge will require recall after 4 minutes. When recall fails, the challenge is repeated again at the last successful interval.

Montessori-based activities were chosen to reinforce healthy eating behaviors because cognitive abilities in dementia patients often resemble those of young children.

For the study, the researchers randomized 90 patients to usual care or to an individualized or non-individualized version of the program. Both versions included sessions lasting 35-40 minutes three times a week. The training focused on eight basic eating behaviors, from remembering mealtimes to swallowing after chewing.

In the individualized program, training was progressively intensified for individual patients if they showed mastery at a given level. The number of sessions also depended on individual patients’ needs. For example, a patient with mild dementia might receive 23 sessions whereas a person with severe dementia might receive 35.

In the non-individualized program, training intensity increased only when more than half the participants had shown mastery. The number of sessions was fixed at 24 over an eight-week period.

About 4 percent to 18 percent in each study group were taking antidepressants, 32 percent to 45 percent were taking antipsychotic medications, and 20 percent to 29 percent were on anti-anxiety drugs.

“The greatest improvement of nutritional status and depressive symptoms resulting from the individualized intervention occurred between the immediate post-training period and the one-month followup,” noted researchers Li-Chan Lin, Ph.D., R.N., of National Yang-Ming University and Hua-Shan Wu, Ph.D., R.N., of Shan Medical University.

Because of this, they suggested that additional “booster sessions” may be helpful in maintaining or increasing the short-term gains.

Source: Journal of Advanced Nursing

Researchers Set Stage for Possible Treatment of Early Stage Alzheimer’s Disease

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

Senior Journal
Melisssa Bloom
 

“Such therapies could preserve brain function longer and delay the appearance of more severe symptoms that leave patients unable to care for themselves.”

In the early stages of Alzheimer’s disease, people struggle with and fail to learn new games, rules or technologies because their cognitive flexibility decreases. The degenerative disease continues with memory loss and the decline of other brain functions.

The researchers worked with mice that had specially designed gene fragments derived from bacteria and from humans that allowed the investigators to control the production of a small peptide. The peptide, called amyloid beta peptide, is a short chain of amino acids. Accumulations of this particular peptide in the brain as lesions called plaques occur early in the progression of Alzheimer’s disease and seem to trigger the early memory problems.

The team regulated the expression of the peptide using antibiotics — when the animals stopped taking the antibiotic, the peptide-producing gene turned on and caused the mice to develop the plaques found in Alzheimer’s patients. After the mice had developed the Alzheimer pathology, the researchers turned the gene back off and observed that the mice showed persistent memory problems that resemble the early stages of the disease.

“This model may be useful to researchers to test drugs that could help with symptoms of early stage Alzheimer’s disease,” Borchelt said.This research is funded by the National Institute of Neurological Disease and Stroke of the National Institutes of Health, and the SantaFe HealthCare Alzheimer’s Disease Research Center of the University of Florida.

About the Author

Melissa Blouin is the Director of News and Publications at the University of Florida Academic Health Center. She was previously the senior director of academic communications at the University of Arkansas.

 

IPSC Technology Lead To Improved Modeling Of Alzheimer's Disease

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

Working with a group from Nagasaki University, a research group at the Center for iPS Cell Research and Application (CiRA) at Japan's Kyoto University has announced in the online publication of Cell Stem Cell that it has successfully modeled Alzheimer's disease (AD) using both familial and sporadic patient-derived induced pluripotent stem cells (iPSCs), and revealed stress phenotypes and differential drug responsiveness associated with intracellular amyloid beta oligomers in AD neurons and astrocytes.

In a study published online in Cell Stem Cell, Associate Professor Haruhisa Inoue and his team at CiRA and a research group led by Professor Nobuhisa Iwata of Nagasaki University generated cortical neurons and astrocytes from iPSCs derived from two familial AD patients with mutations in amyloid precursor protein (APP), and two sporadic AD patients. The neural cells from one of the familial and one of the sporadic patients showed endoplasmic reticulum (ER)-stress and oxidative-stress phenotypes associated with intracellular amyloid beta oligomers. The team also found that these stress phenotypes were attenuated with docosahexaenoic acid (DHA) treatment. These findings may help explain the variable clinical results obtained using DHA treatment, and suggest that DHA may in fact be effective only for a subset of patients.

Using both familial and sporadic AD iPSCs, the researchers discovered that pathogenesis differed between individual AD patients. For example, secreted amyloid beta 42 levels were depressed in familial AD with APP E693 delta mutation, elevated in familial AD with APP V717L mutation, but normal in sporadic AD.

"This shows that patient classification by iPSC technology may contribute to a preemptive therapeutic approach toward AD,'' said Inoue, a principal investigator at CiRA who is also a research director for the CREST research program funded by the Japan Science and Technology Agency. "Further advances in iPSC technology will be required before large-scale analysis of AD patient-specific iPSCs is possible.''