A New Take on What Causes Alzheimer's

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More than a century after German psychiatrist Alois Alzheimer first lectured about the gooey mass of plaques and tangles he noted in a postmortem brain tissue sample, scientists are still debating what causes Alzheimer's disease. 

The majority of scientists have agreed that plaques result from overproduction of beta-amyloid -- a protein found in the cell membrane of neurons. In people with Alzheimer's, this protein accumulates in clumps between brain cells. 

But recently, researchers from Washington University in St. Louis arrived at a new theory: that rising brain levels of beta-amyloid do not mean that patients are making more of it but that they can no longer clear it from their brains as effectively. 

The study. As reported in the journal Science, the investigators tested 24 people, average age 74, and separated them into a group composed of people with minor Alzheimer's disease and another whose members were cognitively normal. Special testing revealed that both groups produced beta-amyloid at the same average rate within the brain. 

The study subjects were then tested to see how the beta-amyloid was cleared from their brains. One of the ways the brain does this is by moving it to the spinal fluid for disposal. The researchers took samples of cerebrospinal fluid by inserting a needle into the subjects' backs and drawing off the fluid that normally surrounds the spinal cord. They found that those with Alzheimer's had decreased clearance of beta-amyloid from the brain to the cerebrospinal fluid -- about 30 percent less than those who were cognitively normal. This suggests that Alzheimer's is associated with disruption of the brain's ability to normally handle the beta-amyloid. 

What it means. Early diagnosis of Alzheimer's has been elusive. But because researchers have uncovered a possible mechanism of early disease development, it is possible that this discovery could lead to both a test for early detection and the development of effective therapies to stop or reverse Alzheimer's memory disruption. They calculate that it would take an adult 10 years to build up enough amyloid in his or her brain to reach the amount typically present in someone with Alzheimer's. 

This knowledge could offer doctors a window of opportunity to diagnose someone long before dementia symptoms develop. Once they learn they are at risk for dementia, people could make more concerted efforts to reduce their personal risk factors for Alzheimer’s. At the same time, pharmaceutical companies could work on targeted medications to halt brain damage before symptoms become irrevocable. 

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Diet Appears to Modulate Alzheimer's Biomarker

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Medscape Today

Results of a new study provide more evidence that diet may modulate the risk for Alzheimer's disease.

In a 4-week diet intervention study, healthy cognitively intact older adults who stuck to a low-saturated-fat, low-glycemic-index diet experienced decreases in cerebrospinal fluid (CSF) levels of β-amyloid 42, a biomarker of Alzheimer's disease risk.

But in a group of older adults with amnestic mild cognitive impairment (aMCI), the healthy diet had the opposite effect, raising CSF levels of this protein.

These observations "made sense to us," Suzanne Craft, PhD, of the Veterans Affairs Puget Sound Health Care System in Seattle, Washington, who worked on the study, told Medscape Medical News.

"That's because in patients with Alzheimer's disease," she explained, "β-amyloid 42 sticks in the brain and so levels are lower in the CSF, and something that is going to reverse that process is going to raise levels in the spinal fluid."

"But for a healthy adult," she said, "it looks like levels get higher and higher over the course of life until, for some people, they reach a tipping point where [β-amyloid 42] begins to stick in the brain. In healthy adults, having levels decrease is actually a healthy pattern."

"It looks like a healthy diet that contains a lot of fruits and vegetables and healthy fats would be important for people who have Alzheimer's disease or conditions that put them at risk for developing Alzheimer's disease," Dr. Craft said.

The study appears in the June issue of the Archives of Neurology.

Mounting Evidence That Diet Matters to the Brain

There is a "fair amount" of evidence starting to accrue in the epidemiologic literature looking at what patterns of diet seem to both be protective and alternatively place someone at greater risk for Alzheimer's disease, Dr. Craft noted.

"That evidence," she said, "is suggesting that a diet like the Mediterranean diet seems to have a protective effect and a diet that has a lot of saturated fat and sugar seems to place you at greater risk."

"Those studies are very important for setting the stage, but what's different about our study is that we actually placed people on a very specific diet and provided every piece of food that they ate for an entire month," the researcher said.

The high-saturated-fat/high-glycemic-index diet included 45% fat (25% saturated fat), 35% to 40% carbohydrates (glycemic index > 70), and 15% to 20% protein. The low-saturated-fat/low-glycemic-index diet included 25% fat (< 7% saturated fat), 55% to 60% carbohydrates (glycemic index < 55), and 15% to 20% protein.

Participants included 20 healthy adults with a mean age of 69.3 years and 29 adults with aMCI and a mean age of 67.6 years. For 4 weeks, 24 participants followed the high-fat diet (9 healthy adults and 15 with aMCI) and 25 followed the low-fat diet (11 healthy adults and 14 with aMCI).

The number of times participants were nonadherent to their assigned diet was "small and comparable among groups," the authors note. The mean nonadherent incidents per week ranged from 1.23 to 1.80 per group.

Effects on β-amyloid "Striking"

As expected, in both groups, the high-fat diet produced unhealthy changes in serum cholesterol and insulin profiles, while the low-fat diet produced healthy changes in these measures.

Notably, the investigators say, the 4-week diet intervention had "striking effects" on β-amyloid 42 concentrations in CSF, the primary outcome measure, and the effects differed by diet and by cognitive status.

In the healthy adults, the high-fat diet increased CSF β-amyloid 42 levels, essentially moving them "in a direction that may characterize a presymptomatic stage of Alzheimer's disease before plaque deposition," the investigators note in their report. The high-fat diet also increased concentrations of the oxidative stress marker F2-isoprostane and lowered insulin levels.

Conversely, in the participants with aMCI, β-amyloid 42 levels were nearly unchanged by the high-fat diet, "possibly because more extreme intervention is needed to exacerbate already-extant pathologic processes," the investigators suggest.

The low-fat diet had beneficial effects in both the healthy participants and the participants with aMCI.

In the aMCI group, it increased β-amyloid 42 concentrations in the CSF, contrary to the pathologic pattern of lowered CSF β-amyloid 42 typically observed in Alzheimer's disease.

In the healthy adults, the healthy diet decreased CSF β-amyloid 42 levels, which may help move them away from the "tipping point" that corresponds with the start of β-amyloid brain deposition, leading eventually to cognitive impairment.

In both groups, the low-fat diet reduced F2-isoprostane concentrations; increased apolipoprotein E, which aids with β-amyloid clearance; and was associated with improved delayed memory, a hallmark cognitive deficit in aMCI and Alzheimer's disease.

In their paper, the researchers say their study provides "converging support" for recent epidemiologic investigations of dietary patterns and Alzheimer's disease risk.

The results, they conclude, support further investigation into the "possibility that consumption of a diet high in saturated fat and simple carbohydrates may contribute to pathologic processes in the brain that increase the risk of Alzheimer's disease, while a diet low in saturated fat and simple carbohydrates may offer protection against dementia and enhance brain health."

The study was supported by grants from the National Institute on Aging and by funding from the Nancy and Buster Alvord Endowment. The authors have no disclosed no relevant financial relationships.

Alzheimer's CSF Test: Useful or Useless?: The Future

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Medscape Today

Andrew Wilner, MD

When a disease-modifying therapy becomes available, early diagnosis of Alzheimer's disease and diagnostic testing will be enthusiastically embraced by patients and neurologists. At that point, the relative advantages and disadvantages, including patient comfort and cost, of CSF testing and other diagnostic testing for Alzheimer's disease, such as genetic testing, neuropsychological testing, and neuroimaging, including magnetic resonance imaging of the temporal lobes, 2-deoxy-2-[F-18] fluoro-D-glucose Positron Emission Tomography (FDG-PET), amyloid radioligand Pittsburgh compound B (PiB), single photon emission computed tomography (SPECT), and their possible combinations, must be evaluated. This day may not be far off; a review of ongoing studies at clinicaltrials.gov reveals multiple candidate drugs under evaluation. For now, neurologists should keep a lumbar puncture tray handy, but they needn't stock up.

Alzheimer's CSF Test: Useful or Useless?: Does It Matter?

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Medscape Today

Andrew Wilner, MD

The second question, is does any additional diagnostic accuracy provided by the CSF test matter? In clinical practice, a laboratory test that confirmed Alzheimer's disease would remove ambiguity in early cases and limit consideration of other disorders that may present with symptoms suggestive of Alzheimer's dementia such as Creutzfeldt-Jakob disease, frontotemporal dementia, normal pressure hydrocephalus, Parkinson's disease with Lewy body dementia, vascular dementia, and depression. In some of these diseases, prompt diagnosis could lead to earlier effective treatment, such as shunting for normal pressure hydrocephalus or antidepressive medications for depression.

The truly persuasive argument for CSF testing in clinical practice would be the reality of a disease-modifying therapy that prevents or slows the progression of Alzheimer's disease. However, not only is there no "magic bullet" for the prevention of Alzheimer's disease, there is no bullet at all.[4] The current treatments offer modest, temporary, and symptomatic improvement at best. For most patients with mild cognitive deficits concerned about the development of Alzheimer's disease, a careful history, physical, and neurological evaluation with close clinical follow-up (a "wait and see" approach) is practical and appears cost effective.

Once people become demented, they can no longer plan for their financial future or dictate their end-of-life care. An early diagnosis of Alzheimer's disease, rather than late, permits a person more autonomy in directing his or her future. However, an early diagnosis of Alzheimer's disease may have negative psychological consequences in an otherwise well-functioning person who must now consider an inexorable decline towards a state of personal oblivion. Consequently, the pros and cons of early diagnosis must be carefully weighed in each individual prior to such a confirmatory test.

The success of clinical trials requires not only that the treatment be effective, but that all subjects have the disease in question. Subjects who have other diseases contaminate the sample and confound results. To improve the likelihood of successful clinical trials for Alzheimer's disease, potential subjects should be considered for CSF and other diagnostic testing. Revision of research criteria for the diagnosis of Alzheimer's disease that includes abnormal biomarkers has been proposed.[5]

Current Indications for CSF Testing
At present, CSF and other biomarker Alzheimer's testing should be reserved for patients who present a diagnostic dilemma, patients with suspected dementia for whom a diagnosis of probable Alzheimer's disease would provide more solace than worry, and patients entering clinical trials.

Alzheimer's CSF Test: Useful or Useless?:

Alzheimer's disease

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Medscape Today

Andrew Wilner, MD

According to a recent editorial, neurologists should be sharpening their lumbar puncture needles in order to obtain cerebrospinal fluid (CSF) to improve their diagnostic accuracy of Alzheimer's disease.[1] The CSF test employs a 2-component mixture model of beta-amyloid 1-42 (AB1-42) and phosphorylated tau protein 181 (P-tau 181P).[2] Model building and validation relied on data from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database (www.loni.ucla.edu/ADNI). The sensitivity of the test was 90% in those with Alzheimer's disease, 72% in those with mild cognitive impairment (MCI), and 36% in controls. The specificity was only 62%.

Commercial assays to diagnose Alzheimer's disease by measurement of CSF beta-amyloid and tau protein have been available for more than a decade. Despite more than 5 million Americans with Alzheimer's disease, and millions more at risk, these CSF tests have yet to be widely adopted by clinical neurologists. At a minimum, there are 2 crucial questions that must be answered before recommending CSF examination as a routine test for Alzheimer's disease.

The first question is does CSF examination improve the accuracy of clinical diagnosis? Clinical diagnostic accuracy of probable Alzheimer's disease according to the standard National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer's Disease and Related Disorders Association (NINCDS-ADRDA) criteria using autopsy as confirmation produces greater than 85% accuracy.[3] It is not clear how much additional precision is added by a positive CSF test in patients with clinically evident Alzheimer's disease. However, CSF testing may allow more accurate earlier diagnosis.

Biomarkers in Cerebrospinal Fluid May Signal Onset of Mild Alzheimer's

DoctorsGuide

Scientists have made a significant step forward in developing a test to help diagnose the early stages of Alzheimer's disease (AD) sooner and more accurately by measuring tau and beta-amyloid proteins in cerebrospinal fluid.

The study, published in the March 17 online issue of the Annals of Neurology, from the Alzheimer's Disease Neuroimaging Initiative (ADNI) not only confirmed that certain changes in biomarker levels in cerebrospinal fluid may signal the onset of mild AD, but also established a method and standard of testing for these biomarkers.

"Research indicates that Alzheimer's pathology causes....read the whole article

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New study identifies link between Alzheimer's disease biomarkers in healthy adults

EurekAlert Amsterdam, The Netherlands -- A study published in the November issue of the Journal of Alzheimer's Disease provides an insight into normal, physiological levels and association between proteins involved in development of Alzheimer's disease. A group of scientists and physicians from the University of Washington and Puget Sound Veterans' Affairs Health Care System in Seattle, in collaboration with groups from the University of Pennsylvania and the University of California San Diego, performed a study in cognitively normal and generally healthy adults, from young to old (age range 21-88 years), of both genders, measuring levels of different brain-derived molecules associated with Alzheimer's disease.

Investigators determined that cerebrospinal fluid (CSF) levels of apolipoprotein E (apoE), one of the most important proteins involved in transfer of fatty substances between different brain cells, are highly correlated with the levels of proteins known to be involved in development of Alzheimer's disease, amyloid precursor protein (APP) and tau. While many studies have previously shown that apoE gene is very important for Alzheimer's disease development, the connection between apoE protein and other relevant CSF markers in healthy adults was not known. Although this type of study cannot establish causal associations, the results strongly suggest that the CSF levels of apoE may explain a significant proportion of the levels of APP- and tau-related biological markers in the healthy human brain, indicating a strong physiological link between apoE, APP and tau. In other words, the study points to a possibility that modulation of the levels of apoE may affect the levels of APP and tau in the brain.

Furthermore, the study has shown that people who have....read the whole story