Here, the age-adjusted Alzheimer's disease mortality rate in Puerto Rico and United States from 1999 to 2004 was analyzed...

PubMed - Am J Alzheimers Dis Other Demen. 2008 Oct-Nov;23(5):462-9.

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This review will discuss the possibility that sex hormone binding globulin (SHBG) plays an active role in the aging process.

PubMed - Horm Metab Res. 2008 Oct 27. [Epub ahead of print]
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Aims: Cube copying measures visuospatial ability, which is often impaired in Alzheimer's disease (AD). Cube copying was examined as an evaluation of cholinesterase inhibitor (ChEI) treatment in AD.

PubMed - Am J Alzheimers Dis Other Demen. 2008 Oct-Nov;23(5):439-46
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This article describes a model of dementia care in which individual care needs are addressed and the social environment is valued as an essential element in care considerations.

PubMed - Am J Alzheimers Dis Other Demen. 2008 Oct-Nov;23(5):430-8.
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Depression is common in patients with neurologic disorders such as Alzheimer disease, stroke, Parkinson disease, and multiple sclerosis. Diagnosing depression in the context of neurologic disease is challenging, given the overlap between many signs and symptoms of depression with those of the neurologic disorders.

PubMed - Am J Med. 2008 Nov;121(11S2):S28-S37.
CLICK HERE TO READ THE FULL ABSTRACT & LINKS TO RELATED ARTICLES

Dr. Cheryl Woodson, you may recall from last week’s post, is a seasoned geriatrician in Chicago Heights, Ill., who has found that she can no longer afford to accept new Medicare patients.

Here’s some of Dr. Woodson’s advice on navigating the caregiving maze, which I culled both from her book, “To Survive Caregiving,” and from observing her during a recent day-long visit to her office.

1. Assisted living, a popular solution for elderly people who cannot live independently, is a “myth,” Dr. Woodson said, “a place for people who don’t exist.” Families often believe these facilities will meet all of their loved ones’ needs, enabling caregivers to focus on jobs and family, only to find this isn’t the case.

2. Squaring a family’s expectations with those legal limits would require a thorough, first-hand assessment of the elderly person’s physical and cognitive health before admission to an assisted living facility. That rarely happens. New residents are admitted based on a report from their current physicians, who may not be qualified to diagnose the early signs of dementia and impending immobility or may sugarcoat the situation in order to help a desperate family.

3. Instead, without verifying the physician’s report or the family’s representations, these facilities may admit residents who already need help with simple tasks like dressing or eating, or will in the very near future, and then charge extra for these services.

4. Coordinating all the services that the assisted living facility doesn’t provide generally falls to one sibling, Dr. Woodson noted, who then becomes overwhelmed, sacrificing more than should be expected. The solution is hiring a geriatric care manager — “They should be called rent-a-daughters,” Dr. Woodson said — adding further to the expense, until the resident and family can no longer afford this kind of accommodation and are forced to consider a nursing home.

5. Most families balk at the prospect of transferring an aging parent to a nursing home because they like the aesthetics of assisted living — the carpeted floors, overstuffed chairs and crystal chandeliers.

6. The doctors who see residents at assisted living facilities are essentially freelancers, not employees, since their fees are paid by Medicare and they also may maintain private practices. So rather than hang around the facility expecting them to answer your questions on the fly, Dr. Woodson suggested calling and arranging to see them “by appointment, not by ambush.”

7. If a parent lives in an assisted living facility, families should closely monitor the monthly pharmacy bill, less for cost than for content. Is Xanax being prescribed for anxiety? There are numerous other remedies available without the potentially dangerous side effects. What about muscle relaxants for arthritic pain? They increase confusion in the elderly and add to the risk of falls; instead, ask for pain medication and/or a heating pad. If the assisted living facility offers to have prescriptions filled and delivered by a local pharmacy — a huge convenience for family members — be sure it’s a pharmacy that insists upon periodic blood work or other tests for drugs that are supposed to be closely monitored.

8. The goal of medical care for the elderly, in Dr. Woodson’s view and the view of every geriatrician I’ve ever interviewed, is to make day-to-day life more comfortable, not to cure illness or extend longevity.

9. Apply similar standards to immunizations and vaccinations. If someone is so ill or disabled that death would be welcome, refuse the vaccine for pneumonia, long known as “the old person’s friend.” But never say no to the shingles vaccine, which can prevent an excruciating rash. “Even if someone was only going to live five more minutes, that’s the one thing I’d suggest,” Dr. Woodson says. “It’s a quality-of-life issue.”

10. Do not assume that the presenting symptom of Alzheimer’s disease will be forgetting words, losing things or other obvious examples of short-term memory loss. Often the first thing a family member will notice is an empty checking account, Dr. Woodson said, because a normally cautious and frugal person has been tricked by a get-rich-quick scheme or other scam. And like missing money, look out for pills missing from those seven-day dispensers that help people with multiple medications keep track of what they’re taking and when.

The New York Times
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Many of you take exception to the notion, expressed here last week by Dr. Cheryl Woodson, that assisted living is a “myth” that promises more than it can deliver to the frail elderly and their families. Interestingly, Dr. Woodson’s provocative observation is echoed in a study and an editorial in the current issue of the Journal of the American Medical Directors Association, both of which suggest that the medical needs of many current assisted-living residents exceed what these facilities can provide and that consumers are not adequately warned of these limitations.

Dr. Matthew K. McNabney, a geriatrician and assistant professor of medicine at Johns Hopkins University, and his fellow researchers reviewed the medical charts of 198 residents at 22 assisted living facilities in central Maryland, then interviewed those residents, their family members and the facility staff. They found that 46 percent of the residents had chronic conditions in three or more broad disease categories, such as those affecting the cardiovascular, pulmonary or endocrine systems. In addition, 25 percent had two or more specific diagnoses, such as congestive heart failure, osteoporosis or Parkinson’s disease, covered by clinical guidelines in use at long-term care facilities.

“As with nursing homes, many assisted living facilities perform admirably,” he wrote in the editorial. “However, overall performance across the country is uneven and often problematic. The public is still not getting a balanced picture of the variability, capabilities and limitations of assisted living. The AL propaganda machine often makes it difficult to engage in a meaningful discussion about reality. Instead, it often shouts down such discourse with the usual platitudes.”

“What almost certainly is needed in the long term,” Dr. McNabney added, “is not pretty decorations, but the capacity and commitment to care for people as their needs progress.”

There are two models of long-term care that experts say more realistically acknowledge the inevitability of decline and dependence among the elderly: CCRCs, or continuing care retirement communities, which require large up-front expenditures as well as high monthly fees; and PACE, an acronym for “program of all-inclusive care for the elderly,” a joint venture of Medicare and Medicaid that operates 42 programs in 22 states and serves low-income clients. We’ll be talking more about them in the future.

The New York Times

CLICK HERE TO READ THE FULL ARTICLE

BACKGROUND: Subjects with Alzheimer's disease (AD) have elevated cortisol levels as a result of hypothalamic-pituitary-adrenal (HPA) axis dysfunction. Acute administration of hydrocortisone has been associated with working memory (WM) performance in young adults.

PubMed - Arq Neuropsiquiatr. 2008;66(3b):619-624.
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BACKGROUND: Disclosure of the diagnosis of Alzheimer's disease (AD) remains a contentious issue, and has been little studied in developing countries.

PubMed - Arq Neuropsiquiatr. 2008;66(3b):625-630.
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This study evaluated the benefits of a Psychoeducational Intervention Program (PIP) on caregiver burden in southern Europe.

PubMed - Int J Geriatr Psychiatry. 2008 Oct 23. [Epub ahead of print]
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This review discusses the utility of transgenic mice as a research tool and their contributions to our understanding of Alzheimer disease.

PubMed - J Biol Chem. 2008 Oct 22. [Epub ahead of print]
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This video article takes the form of a debate between Dr. Morgan and Dr. Landreth on the merits and drawbacks of an Alzheimer's disease vaccine. Click on Supplemental Material to watch the streaming video.

PubMed - J Neuroimmune Pharmacol. 2008 Oct 23. [Epub ahead of print]
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Background/Aims: To examine the incremental effect of patients' dependence on others, on cost of medical and nonmedical care, and on informal caregiving hours over time.

PubMed - Dement Geriatr Cogn Disord. 2008 Oct 22;26(5):416-423. [Epub ahead of print]
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Autopsy cases who had received Abeta vaccine showed clearance of senile plaques, and beneficial effect was shown in patients who had high antibody titers to amyloid plaques. Thus, vaccination is widely accepted as promising therapy for Alzheimer disease.

PubMed - Nippon Rinsho. 2008 Oct;66(10):2008-12.
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In this review we have summarized current proteomics technologies involved in discovery of biomarkers for neurodegenerative diseases, practical considerations and limitations of several major aspects, as well as the current status of candidate biomarkers revealed by proteomics for Alzheimer and Parkinson disease.

PMID: 18938247 [PubMed - as supplied by publisher]
PubMed - Neurobiol Dis. 2008 Sep 26. [Epub ahead of print]
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OBJECTIVES: To evaluate the prevalence of white-coat effect (WCE), and its association with individual anxiety and insight of disease, among older patients evaluated for suspected cognitive impairment.

PMID: 18937278 [PubMed - as supplied by publisher]
PubMed - Int J Geriatr Psychiatry. 2008 Oct 20. [Epub ahead of print]
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OBJECTIVE: This study explored how male and female family caregivers of Alzheimer's disease (AD) patients differ in their use of formal services and informal support and how religiousness may affect such differences.

PMID: 18936242 [PubMed - as supplied by publisher]
PubMed - J Aging Health. 2008 Oct 20. [Epub ahead of print]
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BACKGROUND: There is evidence of increased systemic expression of active GSK3B in Alzheimer's disease patients, which apparently is associated with the formation of senile plaques and neurofibrillary tangles.

PMID: 18932008 [PubMed - as supplied by publisher]
PubMed - Eur Arch Psychiatry Clin Neurosci. 2008 Oct 17. [Epub ahead of print]
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The objective of this study was to determine the relationship between cognitive performance and plasma levels of tHcy and its biological determinants folate and vitamin B(12), and lipids in clinically diagnosed AD patients.

PMID: 18931498 [PubMed - as supplied by publisher]
PubMed - Dement Geriatr Cogn Disord. 2008 Oct 16;26(4):384-390. [Epub ahead of print]
CLICK HERE TO READ FULL ABSTRACT & LINKS TO RELATED INFORMATION

Objectives: There exists little information describing the spectrum and correlations of sexual behaviors manifested by elders with dementia living in residential care.

PMID: 18931496 [PubMed - as supplied by publisher]
PubMed - Dement Geriatr Cogn Disord. 2008 Oct 16;26(4):370-377. [Epub ahead of print]
CLICK HERE TO READ FULL ABSTRACT & LINKS TO RELATED INFORMATION

BACKGROUND: Cross-sectional reports suggest that statin-users are less likely to have Alzheimer disease (AD). Prospective studies have provided inconsistent evidence.

PubMed - J Neurol Neurosurg Psychiatry. 2008 Oct 17. [Epub ahead of print]
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This article provides an update of the available drug therapies for AD and discusses their implications on the oral and dental health of patients.

PubMed - Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2008 Oct;106(4):467-76
CLICK HERE TO READ FULL ABSTRACT & LINKS TO RELATED INFORMATION

This review will focus also on particular classes of AChEIs, namely dual binding site AChEIs, which are being purposely designed to target Abeta aggregation and / or other biological targets that contribute to AD pathogenesis, thus constituting very promising disease-modifying anti-Alzheimer drug candidates.

PubMed - Curr Med Chem. 2008;15(24):2433-55.
CLICK HERE TO READ FULL ABSTRACT & LINKS TO RELATED INFORMATION

PHILADELPHIA — Antonio Vasquez was just 60 when Alzheimer’s disease derailed him.

He lost his job at a Queens bakery because he kept burning chocolate chip cookies, forgetting he had put them in the oven. Then he got lost going to job interviews, walking his neighborhood in circles.

Teresa Mojica of Philadelphia was 59 when she got Alzheimer’s, making her so argumentative and delusional that she sometimes hits her husband. And Ida J. Lawrence was 57 when she started misplacing things and making mistakes in her Boston dental school job.

Besides being young Alzheimer’s patients — most Americans who develop it are at least 65, and it becomes more common among people in their 70s or 80s — the three are Hispanic, a group that Alzheimer’s doctors are increasingly concerned about, and not just because it is the country’s largest, fastest-growing minority.

Studies suggest that many Hispanics may have more risk factors for developing dementia than other groups, and a significant number appear to be getting Alzheimer’s earlier. And surveys indicate that Latinos, less likely to see doctors because of financial and language barriers, more often mistake dementia symptoms for normal aging, delaying diagnosis.

“This is the tip of the iceberg of a huge public health challenge,” said Yanira L. Cruz, president of the National Hispanic Council on Aging. “We really need to do more research in this population to really understand why is it that we’re developing these conditions much earlier.”

It is not that Hispanics are more genetically predisposed to Alzheimer’s, say experts, who say the diversity of ethnicities that make up Hispanics or Latinos make a genetic explanation unlikely.

Rather, experts say several factors, many linked to low income or cultural dislocation, may put Hispanics at greater risk for dementia, including higher rates of diabetes, obesity, cardiovascular disease, stroke and possibly hypertension.

The New York Times
CLICK HERE TO READ THE FULL ARTICLE

MedPage TodayMILAN, Oct. 20 -- More education and mentally challenging employment appear to protect against the cognitive impairment of Alzheimer's disease, researchers here said.

The findings appear to confirm the so-called "brain reserve hypothesis," which suggests that high intelligence, education, and an active lifestyle are associated with a reserve capacity that protects the brain against the effects of aging and disease, according to Valentina Garibotto, M.D., of the Italian National Institute of Neuroscience, and colleagues.

But it remains unclear whether the reserve is a genetic endowment that also leads to higher education and employment or whether such mental challenges create the reserve, Dr. Garibotto and colleagues said in the Oct. 21 issue of Neurology.

"The theory is that education and demanding jobs create a buffer against the effects of dementia on the brain, or a cognitive reserve," Dr. Garibotto said.

For people with such a history, "their brains are able to compensate for the damage and allow them to maintain functioning in spite of damage," she said.

Indeed, in the study, people with more education and more demanding jobs tended to have more brain damage for a given level of impairment -- indicating, the researchers said, that they cope better with the disease than their less educated counterparts.

On the other hand, among the probable Alzheimer's patients, higher educational level was associated -- for the same level of clinical impairment -- with lower blood glucose in the right temporo-parietal association cortex and the precuneus. The association was significant at P<0.01.>

There are two possible explanations of the findings, Dr. Garibotto said.

"The brain could be made stronger through education and occupational challenges," she said, "or genetic factors that enabled people to achieve higher education and occupational achievement might determine the amount of brain reserve."

But, she added, it isn't possible yet to say which explanation holds true.

MedPage Today

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White matter hyperintensities (WMH) are frequently seen on T(2)-weighted MRI scans of elderly subjects with and without Alzheimer's disease.

Brain. 2008 Oct 16. [Epub ahead of print]
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Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York, USA.

Alzheimer disease (AD) is the most common cause of dementia in adults. The current therapy for AD has only moderate efficacy in controlling symptoms, and it does not cure the disease. Recent studies have suggested that abnormal hyperphosphorylation of tau in the brain plays a vital role in the molecular pathogenesis of AD and in neurodegeneration. This article reviews the current advances in understanding of tau protein, regulation of tau phosphorylation, and the role of its abnormal hyperphosphorylation in neurofibrillary degeneration.

PMID: 18855662 [PubMed - in process]
Curr Med Chem. 2008;15(23):2321-8.
CLICK HERE TO READ THE FULL ABSTRACT & RELATED INFORMATION

Laboratori de Química Farmacèutica (Unitat Associada al CSIC), Facultat de Farmàcia, Universitat de Barcelona, Av.

The therapeutic arsenal for the treatment of Alzheimer's disease (AD) remains confined to a group of four inhibitors of AChE and one NMDA receptor antagonist, which are used to provide a relief of the very late symptoms of the dementia, i.e. the cognitive and functional decline.....

This review will focus also on particular classes of AChEIs, namely dual binding site AChEIs, which are being purposely designed to target Abeta aggregation and / or other biological targets that contribute to AD pathogenesis, thus constituting very promising disease-modifying anti-Alzheimer drug candidates.

PMID: 18855672 [PubMed - in process]
Curr Med Chem. 2008;15(24):2433-55
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Wolfson Centre for Age-Related Diseases, Guy's Campus, King's College London.

Neuropsychiatric symptoms are frequent in people with dementia, result in distress for the people experiencing them and their caregivers, and are a common precipitant of institutional care. The safe and effective treatment of these symptoms is a key clinical priority, but is a long way from being achieved. Psychological interventions are recommended as the first line treatment strategy in most good practice guidelines, and there is emerging evidence of efficacy for agitation and depression.

PMID: 18925489 [PubMed - in process]
Int Rev Psychiatry. 2008 Aug;20(4):396-404.
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SAN DIEGO, Oct. 14 -- High-dose vitamin B supplements reduced homocysteine levels but did not slow Alzheimer's disease progression, researchers here found in a large placebo-controlled trial.

After 18 months of treatment, patients taking high doses of vitamins B6 and B12 as well as folic acid showed the same degree of cognitive decline compared with baseline as those assigned to placebo, reported Paul Aisen, M.D., of the University of California San Diego, and colleagues in the Oct. 15 issue of the Journal of the American Medical Association.

Participants in the vitamin group also showed a significantly higher frequency of depressive symptoms, seen in 27.9% compared with 17.8% of the placebo group (P=0.02). Blurred vision and hyperhidrosis also appeared more common with vitamin supplements, but the differences missed statistical significance (P=0.7 and 0.53, respectively).

"Our study does not support the treatment of individuals with mild to moderate Alzheimer's disease and normal vitamin levels with B vitamin supplements," Dr. Aisen and colleagues concluded.

The study was prompted by earlier findings that blood homocysteine levels are elevated in patients with Alzheimer's disease and that B vitamin supplements can lower homocysteine levels.

But there was not even a hint that vitamin supplements slowed participants' cognitive decline by any measure used in the study:

--Alzheimer Disease Assessment Scale cognition scores increased 6.54 points (SD 8.17) in the placebo group after 18 months, compared with 7.38 points (SD 9.72) in the vitamin supplement group.

--Mini-Mental State Exam scores decreased 3.08 points (SD 4.46) in the placebo group versus 2.65 points (SD 4.56) with supplements.

--Clinical Dementia Rating scores increased 2.51 points (SD 2.57) with placebo compared with 2.58 points (SD 2.45) in the supplement group.

--Activities of daily living scores on the Alzheimer Disease Cooperative Study index decreased 10.00 points (SD 11.09) with placebo versus 10.96 points (SD 12.36) with supplements.

Dr. Aisen and colleagues stopped short of ruling out any benefit from vitamin B supplements for anyone.

"Randomized studies in individuals without dementia have yielded conflicting results; supplementation may be useful in older individuals with relatively high homocysteine levels," they wrote. "The identification of groups that may benefit from such treatment remains an important goal."

They said it was possible that supplements might be more effective if begun while cognition is still intact. "Individuals with established cognitive impairment may be refractory to treatment," Drs. Clarke and Bennett suggested.

But until future research identifies populations or circumstances in which supplements are beneficial, "there is insufficient evidence to justify routine use of homocysteine-lowering vitamin supplements for the prevention of Alzheimer disease and cognitive decline among individuals with normal vitamin status," they said.

MedPage Today
CLICK HERE TO READ THE FULL ARTICLE

Laboratori de Química Farmacèutica (Unitat Associada al CSIC), Facultat de Farmàcia, and Institut de Biomedicina (IBUB), Universitat de Barcelona, Av. Diagonal 643, E-08028-Barcelona, Spain.

The therapeutic arsenal for the treatment of Alzheimer's disease (AD) remains confined to a group of four inhibitors of AChE and one NMDA receptor antagonist, which are used to provide a relief of the very late symptoms of the dementia, i.e. the cognitive and functional decline.

This review will focus also on particular classes of AChEIs, namely dual binding site AChEIs, which are being purposely designed to target Abeta aggregation and / or other biological targets that contribute to AD pathogenesis, thus constituting very promising disease-modifying anti-Alzheimer drug candidates.

PMID: 18855672 [PubMed - in process]
PubMed
Curr Med Chem. 2008;15(24):2433-55.
CLICK HERE TO READ FULL ABSTRACT

Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York, USA.

Alzheimer disease (AD) is the most common cause of dementia in adults. The current therapy for AD has only moderate efficacy in controlling symptoms, and it does not cure the disease. Recent studies have suggested that abnormal hyperphosphorylation of tau in the brain plays a vital role in the molecular pathogenesis of AD and in neurodegeneration. This article reviews the current advances in understanding of tau protein, regulation of tau phosphorylation, and the role of its abnormal hyperphosphorylation in neurofibrillary degeneration. Furthermore, several therapeutic strategies for treating AD on the basis of the important role of tau hyperphosphorylation in the pathogenesis of the disease are described. These strategies include (1) inhibition of glycogen synthase kinase-3beta (GSK-3beta), cyclin-dependent kinase 5 (cdk5), and other tau kinases; (2) restoration of PP2A activity; and (3) targeting tau O-GlcNAcylation. Development of drugs on the basis of these strategies is likely to lead to disease-modifying therapies for AD.

PMID: 18855662 [PubMed - in process]
PubMed
Curr Med Chem. 2008;15(23):2321-8.
CLICK HERE TO READ FULL ABSTRACT

Przychodnia Chorób Zawodowych Wsi, Instytut Medycyny Wsi, 20-950 Lublin, ul. Jaczewskiego 2.

Patients with dementia, especially with dementia in the course of Alzheimer's disease require long-time care. The aim of the research was to assess how caregivers deal with everyday care problems, especially the psychical and social ones. The study was conducted in 1999 by the method of anonymous inquiry in the group of 42 caregivers, mostly members of Lublin's Alzheimer Association. The caregivers are children (53.6%) or spouses of patients (39.8%). In 61% of cases patient lives with the carer's family. 72% of our respondents consider their work as very hard. The care takes them seven days a week, 77% of carers have no possibility of rest. Almost half of respondents (47%) constantly feel depressed and tired. 15% claim that they hardly cope with nursing. 39% of caregivers have the feeling of deep, internal exhaustion.

PMID: 18853662 [PubMed - in process]
PubMed
Przegl Lek. 2008;65(6):304-7
CLICK HERE TO READ FULL ABSTRACT

Department of Neurology, Emory University School of Medicine, 1841 Clifton Road NE, Atlanta, GA 30329, USA. mevatt@emory.edu

BACKGROUND: A role for vitamin D deficiency in Parkinson disease (PD) has recently been proposed.

CONCLUSIONS: This report of 25(OH)D concentrations in a predominantly white PD cohort demonstrates a significantly higher prevalence of hypovitaminosis in PD vs both healthy controls and patients with AD. These data support a possible role of vitamin D insufficiency in PD. Further studies are needed to determine the factors contributing to these differences and elucidate the potential role of vitamin D in pathogenesis and clinical course of PD.

PMID: 18852350 [PubMed - in process]
Arch Neurol. 2008 Oct;65(10):1348-52.
CLICK HERE TO READ FULL ABSTRACT

Department of Neurosciences, University of California, San Diego, 9500 Gilman Dr, M/C 0949, La Jolla, CA 92093, USA. paisen@ucsd.edu

CONTEXT: Blood levels of homocysteine may be increased in Alzheimer disease (AD) and hyperhomocysteinemia may contribute to disease pathophysiology by vascular and direct neurotoxic mechanisms. Even in the absence of vitamin deficiency, homocysteine levels can be reduced by administration of high-dose supplements of folic acid and vitamins B(6) and B(12). Prior studies of B vitamins to reduce homocysteine in AD have not had sufficient size or duration to assess their effect on cognitive decline.

CONCLUSION: This regimen of high-dose B vitamin supplements does not slow cognitive decline in individuals with mild to moderate AD.

PubMed
JAMA. 2008 Oct 15;300(15):1774-83.
CLICK HERE TO READ FULL ABSTRACT & RELATED INFORMATION

One tiny brain cell is all it takes to restore voluntary movement of paralysed muscles, scientists in the United States reported Wednesday.

In experiments pointing to new treatments for paralysis caused by spinal cord injury or stroke, monkeys learned within minutes to harness the power of a single neuron to activate muscles immobilised by drugs.

There are some 100 billion neurons in the human brain, and the study suggests an unsuspected degree of flexibility in the kinds of tasks they can perform.

"Nearly every neuron we tested could be used to control this type of stimulation," Chet Moritz, lead author and a researcher at the University of Washington, told journalists in a conference call.

If a monkey can do it, a human should be able to do it even better, he said.

Clinical trials, however, are at least several years away, perhaps longer, Moritz added.

Spinal cord injuries cripple hundreds of thousands of people worldwide every year, rendering the simplest of actions -- opening a door, scratching an itch, drinking a glass of water -- frustratingly difficult, or simply impossible.

Those afflicted with the most severe form of paralysis, known as lock-in syndrome, are fully conscious prisoners inside a body that no longer responds to commands.

While the brain activity that would normally result in a voluntary movement is still present, the instructions simply don't reach the muscles.

Moritz and two colleagues at the University of Washington found a way to bypass the kind of nerve damage that can result in such paralysis.

They first connected electrodes to individual neurons inside the motor cortex of monkey's brain and recorded the electrical activity.

These signals were then routed in real-time to a computer, and from there through a stimulator to another set of electrodes attached directly to wrist muscles that had been artificially blocked further up the arm along the normal neural pathway.

Because little processing power is needed, the computer is the size of a cell phone, and can be attached to the animal's body.

Future versions will be wireless and small enough to implant directly in the body, the researchers said.

The monkey had already mastered a simple video game, grasping targets shown on a video screen with a control device manipulated by a single hand.

"But once he was paralysed, the only way to move his wrist was to change the activity of individual neurons in his brain," Moritz explained.

On average it took about 10 minutes for the monkeys to "train" the neuron well enough to play the video game again.

"The brain can very rapidly learn to control new cells and use them to generate movements," said co-author Eberhard Fetz.

Earlier experiments enabling monkeys to manipulate prosthetic devices or computer cursors using only electrical impulses coming from the brain were based on a fundamentally different premise, according to the new study.

"They tried to read the mind of the money and figure out what he was planning to do," a technique that required massive computing power, said Moritz.

"Our approach is to recreate the raw connectivity between single neurons in the brain and muscles, and let the monkey's nervous system learn how to use that connectivity."

This is also the first study to show that a one neuron can control a muscle -- and possibly a whole group of muscles.

Electrodes connected to a single location in the spinal cord below an injury may be able to activate 10 or 15 muscles that are already precisely balanced for, say, grasping a coffee mug or walking, the researchers said.

And if a stroke has damaged the motor cortex, patients might be able to commandeer other brain cells that do not usually play a role in controlling muscles.

Several obstacles remain, however, before this new technique can be tested in humans, he said.

To avoid infections, the system would have to become fully implantable so that no wires passed through the skin. And electrodes would need to be made more stable so that they could record the activity of neurons over a period of years, rather than weeks.

Breitbart.com

CLICK HERE TO READ FULL STUDY & RELATED INFORMATION

Department of Neurology, Alzheimer Centre, VU University Medical Center, PO Box 7057, De Boelelaan 1118, 1007 MB Amsterdam, Noord Holland, The Netherlands; Department of Clinical Neurophysiology, VU University Medical Centre, PO Box 7057, 1007 MB Amsterdam, The Netherlands.

OBJECTIVE: We examined the relation between Apolipoprotein E epsilon4 allele (ApoE epsilon4) genotype and functional connectivity measured by Electroencephalography (EEG) in patients with Alzheimer's disease (AD) and patients with subjective complaints (SC).

SIGNIFICANCE: The observed increase in SL in both AD and patients with SC carrying ApoE epsilon4 suggests a strong genetic impact of ApoE epsilon4 on brain function.

PMID: 18848805 [PubMed - as supplied by publisher]
Clin Neurophysiol. 2008 Oct 9. [Epub ahead of print]

CLICK HERE TO READ FULL ABSTRACT & RELATED INFORMATION

From the Department of Psychiatry, University of Pittsburgh School of Medicine, Western Psychiatric Institute and Clinic (AJB, MAD, CFR); and Carnegie Mellon University (VA, JF, SS, HW), Pittsburgh, PA.

The number of older Americans afflicted by Alzheimer disease and related dementias will triple to 13 million persons by 2050, thus greatly increasing healthcare needs. An approach to this emerging crisis is the development and deployment of intelligent assistive technologies that compensate for the specific physical and cognitive deficits of older adults with dementia, and thereby also reduce caregiver burden.

PMID: 18849532 [PubMed - as supplied by publisher]
Am J Geriatr Psychiatry. 2008 Oct 10. [Epub ahead of print]

CLICK HERE TO READ FULL ABSTRACT & RELATED INFORMATION

Department of Pharmacological and Pharmaceutical SciencesCollege of Pharmacy, University of Houston, Houston, Texas.

BACKGROUND: Alzheimer's disease (AD) is a degenerative disorder that leads to progressive cognitive decline. Alzheimer's disease develops as a result of over-production and aggregation of beta-amyloid (Abeta) peptides in the brain. The reason for variation in the gravity of symptoms among AD patients is unknown and might result from patient-related factors including lifestyle. Individuals suffering from chronic stress are at an increased risk for developing AD. This study investigated the effect of chronic psychosocial stress in Abeta rat model of AD.

CONCLUSIONS: Chronic stress significantly intensified Abeta-induced deficits of short-term memory and E-LTP by a mechanism involving decreased CaMKII activation along with increased calcineurin levels.

PMID: 18849021 [PubMed - as supplied by publisher]
Biol Psychiatry. 2008 Oct 10. [Epub ahead of print]

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Department of Pharmaceutical Sciences, College of Pharmacy, University of Kentucky Academic Medical Center, 511C Pharmacy Building, 725 Rose Street, Lexington, KY 40536-0082, USA; Graduate Center for Toxicology, University of Kentucky Academic Medical Center, Lexington, KY 40536-0305, USA.

The objective was to estimate oral Al bioavailability from tea infusion in the rat, using the tracer (26)Al. (26)Al citrate was injected into tea leaves.

Further testing of the hypothesis that Al contributes to Alzheimer's disease may be more warranted with studies focusing on total average daily food intake, including tea and other foods containing appreciable Al, than drinking water.

PMID: 18848597 [PubMed - as supplied by publisher]
Food Chem Toxicol. 2008 Sep 21. [Epub ahead of print]

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Genetic studies are a critical source of knowledge about neurodegenerative diseases. The identification of families with an autosomal dominant pattern of inheritance has proven crucial in improving our care of patients with conditions such as Alzheimer disease (AD) and Parkinson disease. This work has led to improvements in diagnostic accuracy, a better understanding of the biologic mechanisms underlying disease, and most importantly, the identification of targets for therapeutic intervention. Recently, genetic studies of patients with frontotemporal dementia (FTD) have proven to be very fruitful. Two distinct, genetically determined causes have been defined in the last decade. These include the locus of the gene coding for the microtubule-associated protein tau (MAPT) on chromosome 17,1 and within the last 2 years, the gene coding for progranulin (GRN), also on chromosome 17.2,3

Despite these remarkable advances, the glass remains half empty. Why? There is substantial reason to be optimistic about our ability to identify the cause of FTD in up to 27% of patients with an autosomal dominant family history. However, the cause of disease remains a mystery in 73% of patients with FTD. Many pieces of the puzzle remain to be found. Very few studies have pursued interacting genetic factors, for example, and even fewer studies have examined environmental risk factors for FTD and more complex interactions between genetics and the environment. Much biomarker work is needed to identify the histopathologic abnormalities during life of patients with sporadic FTD who show accumulations of the same aberrant proteins at autopsy. This would allow treatments developed for familial FTD to be administered safely and confidently to patients with similar sporadic diseases.

The report of Seelaar et al. provides us with an important yardstick indicating our remarkable success in identifying the cause of FTD in an impressively large percentage of these patients. They also point us in informative directions for future work that can identify the cause of disease in some additional familial patients with FTD. Before breaking out the champagne, however, we should consider the large amount of work that remains before we can improve the care of all patients with FTD.

Despite many promising leads, new treatments for Alzheimer's are slow to emerge. Future treatments will likely focus on stopping the disease in people at risk.

Alzheimer's treatments consist mainly of medications that stabilize cognitive function, if only for a short period of time. These drugs stage a holding action, primarily postponing further cognitive declines.

But the Alzheimer's treatments of the future will focus more on preventing the disease or halting its progress in its earliest stages. The following treatment options are among the strategies currently being studied.

Alzheimer's vaccine

Immunization can reduce the number of amyloid plaques — clusters of abnormal cells associated with Alzheimer's disease — in the brain. But a human trial of an Alzheimer's vaccine was halted when several participants developed brain inflammation.

Secretase modulators

Secretase-modifying drugs might block the action of the clumping enzymes, or activate the nonclumping enzyme.

Certain anti-inflammatory drugs — including ibuprofen (Advil, Motrin, others), naproxen sodium (Aleve) and indomethacin (Indocin) — appear to modify how one of these enzymes works, so that it doesn't produce fragments that clump. One of the most promising drugs being studied in this group is tarenflurbil (Flurizan).

Antibiotics

A three-month course of antibiotics, specifically doxycycline and rifampin, reduced the rate at which cognitive problems worsened in a group of people who had mild to moderate Alzheimer's disease. The antibiotics appear to interfere with the development of amyloid plaques in the brain.

Hormones

Early studies indicated that hormone replacement therapy, typically prescribed to ease menopausal symptoms, might protect women over the age of 65 against Alzheimer's. But more recent studies not only refute these findings but also suggest that this hormone therapy might even increase the risk of dementia.

In men, low testosterone levels have been linked to increased risk of Alzheimer's disease. Researchers are investigating whether testosterone supplements might help men who have Alzheimer's or are at risk of the disease, but the results have been mixed.

Timeline for answers

New Alzheimer's treatments take time to develop, and then even more studies are needed to establish a treatment's safety and effectiveness. But all this time and effort will eventually pay off. Most researchers expect to see major progress in the treatment and prevention of Alzheimer's in the next few decades.

MayoClinic.com
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Heredity, genetics make disease more likely, but how much isn't clear

For adult children of patients with Alzheimer’s disease, the diagnosis can be devastating — and not just because of what it means for their parents.

Along with concerns about caregiving and grief over the loss of the mother or father they knew, there’s another, more private fear: What if I get it, too?

“I think about it all the time,” said Julie Winokur, 44, a videographer from Montclair, N.J., who chronicled her father’s decline into dementia and its effects on her family. “It’s a terrifying thing to me.”

But even as scientists say they may be getting closer to predicting who may develop the mind-robbing disorder, thanks to new research into biomarkers, heredity and genetics, many children of people who suffer or died from the disease say they wouldn’t want to know.

“My feeling is I’d only want to know if there’s something I can do about it,” said Winokur.

Right now, that’s not the case, Alzheimer’s experts concede. There’s virtually no known cause, no cure and no prevention for the disease that causes memory loss and mental deterioration and affects some 5.2 million people in the U.S. and some 27 million people worldwide.

“I don’t know of anything that has been documented to prevent the onset of this disease,” said Dr. Thomas Bird, a neurologist and Alzheimer's disease researcher at the University of Washington in Seattle. “The advice you get is the advice you’d give to anybody to live a good, healthy lifestyle: Watch your weight, watch your blood pressure, eat a balanced diet.”

Recommendations for ways to predict the disease are even more vague. Perhaps 5 percent of Alzheimer’s cases are caused by a rare genetic mutation responsible for early onset of the disorder that usually strikes after 65. For the rest, scientists have proposed analyzing everything from blood, saliva, skin cells, urine and brain scans to detect early signs of the disorder, with no irrefutable results.

Even the most reliable marker of risk, the apolipoprotein E-e4 gene, known as ApoE4, doesn’t determine for sure whether a person will develop Alzheimer’s. Many people with the gene do get the disease, but many don’t, prompting most experts to advise against screening, Bird said.

That leaves offspring of one or both parents with dementia in limbo, focusing on doing anything they can to stave off Alzheimer’s, even when there’s no clear agreement on what that might be. That can range from working crossword puzzles and gulping antioxidants to engaging in new forms of physical exercise, techniques suggested — but not proven — to prevent the disease.

“We’re being much more vigilant about our exercise,” said Karen Moldt, 54, of the oldest of five siblings in Cary, N.C., who were “shell-shocked” when their father was diagnosed with Alzheimer’s four years ago. “One of my brothers who is right-handed started doing things with his left hand.”

Genetics, heredity boost risk

Still, recent research into genetics and heredity suggests that children like Winokur and Moldt have reason to worry.

Just this summer, Dr. Piero Antuono and a team of scientists at the Medical College of Wisconsin reported that healthy offspring of Alzheimer’s patients who carry the ApoE4 gene show declines in brain function that are detectable long before any clinical symptoms appear.

And last spring, Bird and a team of researchers at the University of Washington revealed that children with two parents who have Alzheimer’s disease are far more likely to get the disease themselves.

In the study of 111 families in which two parents were diagnosed with Alzheimer’s, more than 22 percent of the adult children also developed the disease. That compares to about 13 percent expected in the general population, according to the national Alzheimer's Association. The risk rose with age, affecting 30 percent of children older than 60 and nearly 42 percent of those older than 70.

“I pretty much though that my odds of getting it had to be higher than anybody walking down the street,” said Gayle Dorman, 63, of Tacoma, Wash., a study participant who lost both parents to Alzheimer’s a decade ago.

Increasingly, families like Dorman’s are confronting what neurologist Dr. Daniel I. Kaufer calls the “double-parent dementia dilemma.”

“The way I convey this to children is that it’s a double whammy,” said Kaufer, who directs the Memory and Cognitive Disorders program at the University of North Carolina School of Medicine. “They have the burden of care and the burden of risk.”

‘Oh my god, I hope this doesn't happen to me’
Coping with that burden isn’t easy for family members confronting their own future, said Dr. Zoe Lewis, a palliative care specialist and author of a new book, “I Hope They Know: The Essential Handbook on Alzheimer’s Disease and Care.”

“It is literally the collective fear of anyone, anywhere: Oh my god, I hope this doesn’t happen to me,” Lewis said.

As patients watch their parents spiral downward, often over several years or even decades, they can't help but wonder whether that's the fate they face.

"The fear is that you'll lose your mind and you won't be treated well," Lewis explained.

That fear permeates daily life, making children vigilant for signs of dementia, said Dorman. “For me, it’s pretty scary when I forget where I parked my car. I think, ‘Here it is, here I go.’”

Winokur said she quizzes herself constantly, testing to see whether she remembers people’s names and what they were wearing.

Many children of parents with dementia say they’ve considered confirming their risk by being screened for the ApoE4 gene — and then rejected the idea. “Right now, I don’t know if I’d want to know,” Dorman said.

Others, however, think the information could be valuable. “You could just plan better. If you have a ticking time bomb, you’d want to know, wouldn’t you?” said Mike Sanchez, 37, of Santa Ana, Calif. His 82-year-old father has had Alzheimer’s disease for more than a decade.

Most children of dementia patients are able to put their fear in perspective, said Bird, the University of Washington researcher whose own mother died of Alzheimer's disease.

"I know that I'm at risk for it. Everybody who gets older is at risk. My risk is higher than average," he said. "But I don't feel there's anything more than I could do than I do to prevent it. I don't worry about a disease that I can't prevent."

But at least one son of an Alzheimer’s patient had his worry confirmed in the worst way: By developing signs of the disease himself.

“Within the last nine months, when I try to think of a word, I draw a blank. I’ll know I’m looking for a word and can’t find it,” said Francis, a 59-year-old mechanical engineer from South Carolina who watched his mother succumb to the disease.

He asked to be identified only by his middle name because he hasn’t told his children or his employer that he likely has early-onset Alzheimer’s disease. He has begun taking donepezil, popularly known as Aracept, one of a handful of drugs aimed at slowing cognitive decline.

Francis is clear that he does not want his wife and grown children burdened by his disease. He said he wouldn’t think of asking them to care for him at home if the disease gets worse.

“If it happens to me, I will probably divorce my wife, become indigent and let the government take care of me,” he said.

That’s a stark contrast to Winokur, who said the care she provided keeping her father at home should serve as a model for her children.

“I would really pray that by example, that’s just something you can expect,” she said. “I would definitely want to stay at home. I fulfilled what I would want.”

Researchers like Antuono, who also lost his mother to Alzheimer's, expect to have a reliable treatment for Alzheimer's within a decade.

"In 10 years we'll have an intervention that willl compress the first symptoms of the disease all the way to end," he said, noting that it likely will make the disease a chronic condition, but will not cure the disorder. "A cure to get rid of this altogether? That might be left to the next generation."