Alzheimer's research update
July 20, 2008
Medicine | Science

Update on Alzheimer's: Diagnostic techniques, News and Research

So much new research has been published lately it's hard to know where to start. I'll summarize first a bit of the current understanding of Alzheimer's diagnosis, and then move on to what's been happening lately in the areas of research and treatment.
  • Section I - Diagnosis: the current state of Alzheimer's diagnostic techniques
    More after the jump...
    Ads by Google
    Posted by ellen at July 20, 2008 10:39 AM
  • Section II - Treatment and ongoing research

    Diagnosis: The current state of Alzheimer's diagnostic techniques:

    Until recently the only way an accurate diagnosis of Alzheimer's could be made was to wait for the patient to die, then examine their brain for Alzheimer's type pathologies. That began to change several years ago, when better diagnostic tools began to be developed.

    from: Detecting Alzheimer's Early

    Optical Scientists, Psychiatrists Develop Minimally Invasive Eye Test for Alzheimer's

    December 1, 2005
    Building upon a recent discovery that the same Alzheimer's disease process that goes on in the brain also occurs in the eye, researchers have developed a pair of optical tests that can determine the presence of amyloid beta proteins -- found in all Alzheimer's patients -- in the lens of the eye. A device called an interior laser ophthalmoscope can pick up the presence of the amyloid protein.

    from Discoveries and Breakthroughs inside Science

    In 2006, a study was published where EEG analysis was successfully used to distinguish early signs of Alzheimer's from normal aging:

    from: Predicting Alzheimer's
    Psychiatrists Can Predict Onset of Alzheimer's with New EEG Test
    March 1, 2006

    "Using new computer software that analyzes EEG data, psychiatrists can now better distinguish early signs of Alzheimer's from normal aging, by spotting marked differences between the left and right sides of the brain. Diagnosing Alzheimer's early can be vital because new drugs can now slow the progression the disease. The new technique is cheaper and less invasive than using MRIs or PET scans for the same diagnosis.

    Leslie Prichep, an associate director of the Brain Research Laboratories of the Department of Psychiatry at New York University School of Medicine, says, "Going from the squiggly lines to a description of those events, we are then comparing those numbers to the expected numbers for the age of the individual."

    Using new computer software that converts the EEG scan into numbers, psychiatrists can more easily determine normal aging vs. early signs of dementia. For instance, the left EEG shows the left and right sides of the brain are normal size, shape and similar between regions, suggesting no dementia. The right EEG, however, shows big differences between left and right sides -- indicating signs of future dementia. Prichep says this is significant, because there are now drugs that show to be very useful in stopping and slowing the progression of dementia..."

    from Discoveries and Breakthroughs inside Science

    From : "Quantitative EEG and electromagnetic brain imaging in aging and in the evolution of dementia"
    Annals of the New York Academy of Sciences, 2007 Feb;1097:156-67

    We have recently reported results from initial quantitative electroencephalography (QEEG) evaluations of normal elderly subjects (with only subjective reports of memory loss), predicting future cognitive decline or conversion to dementia, with high prediction accuracy (approximately 95%). In this report, source localization algorithms were used to identify the mathematically most probable underlying generators of abnormal features of the scalp-recorded EEG from these patients with differential outcomes. Using this QEEG method, abnormalities in brain regions identified in studies of AD using MEG, MRI, and positron emission tomography (PET) imaging were found in the premorbid recordings of those subjects who go on to decline or convert to dementia

    from: FDG-PET Imaging Allows Early Detection of Alzheimer's, Other Dementia Types

    Caroline Cassels
    Medscape Medical News 2008.
    "April 3, 2008 -- New research shows positron emission tomography (PET) in combination with the radiotracer flurodeoxyglucose (FDG) can accurately detect and classify different types of dementia in up to 94% of cases -- a finding that investigators say could lead to better dementia treatment and possibly even prevention.
    In a large multicenter study that included 7 centers in the United States and Europe, investigators at the New York University (NYU) School of Medicine used optimized FDG-PET analysis techniques to measure glucose metabolism in different regions of the brain and successfully distinguish patients with mild cognitive impairment (MCI), Alzheimer's disease (AD), dementia with Lewy bodies (DLB), and frontotemporal dementia (FTD).

    "We used FDG-PET to measure how efficiently the brain utilizes glucose and observed distinct regional patterns of hypometabolism in patients with different types of dementia," the study's first author, Lisa Mosconi, PhD, told Medscape Neurology & Neurosurgery...

    The study is published in the March issue of the Journal of Nuclear Medicine."

    from: Accurate, Noninvasive Diagnosis of Alzheimer's Disease Is Possible (CME)
    News Author: Caroline Cassels
    CME Author: Désirée Lie, MD, MSEd

    ...In a study published in the December 21, 2006, issue of The New England Journal of Medicine (N Engl J Med. 2006;355:2652-2663), researchers at the University of California Los Angeles demonstrated that FDDNP-PET... scanning can distinguish between AD, mild cognitive impairment, and subjects with no cognitive impairment.

    "Considering the importance of a definitive diagnosis of Alzheimer's disease at the earlier stages of the disease, I believe these results could have significant impact," principal investigator Jorge Barrio, PhD, told Medscape.

    The next steps, said Dr. Barrio will be to confirm these findings and then to test FDDNP-PET in intervention trials. The University of California Los Angeles, he said, has a number of studies underway looking at potential early therapies. One of these includes the use of curcumin, the yellow pigment in curry spice, which was shown by Dr. Barrio's colleagues to dissolve beta-amyloid plaques in the brains of transgenic mice.

     

    Bay Area med centers develop tests for dementia
    Erin Allday, Chronicle Staff Writer
    Saturday, July 19, 2008

    At UCSF, geriatric specialists last month introduced plans to use Internet staples like YouTube and Facebook to help people recognize the earliest signs of dementia. Along with basic information on degenerative neurological diseases, the Web sites incorporate videos, made by both health care professionals and the families of patients, with detailed descriptions of the various forms of dementia, including symptoms that most people wouldn't recognize.
    "A lot of patients and their families go to the Internet for information, and there isn't a lot of reliable information there for them," said Dr. Bruce Miller, director of UCSF Memory and Aging Center. "I often find that it's not the doctor who makes the correct diagnosis, it's the family. Family members are puzzled by someone who was doing fine and suddenly isn't."

    Researchers at UCSF and UC Berkeley are working on scanning techniques that would help doctors recognize signs of dementia in the brain before symptoms even appear. The scans would look for clumps of the protein called amyloid, which builds up like plaque in the brains of people with dementia.

    Treatment and ongoing research:

    First, a bit of controversy regarding the dominant research focus on one treatment target (amyloid plaques) to the exclusion of other possibly promising treatments:

    In a Newsweek blog, Sharon Begley writes,

    July 03, 2008 1:54 The Scandal That is Alzheimer's Research Sharon Begley

    Of all the columns I've written, no topic has brought more agonized, heartfelt and desperate-sounding emails than Alzheimer's disease. Back in 2004, I wrote three columns (when I was at The Wall Street Journal) on how one particular theory of what causes this awful disease--and therefore the best approach for treating it--has had the field in a headlock, censoring competing theories. That closed-mindedness, I quoted scientists as saying, had a lot to do with why there is not only no cure or preventive for Alzheimer's, but not even a treatment that slows down the inexorable cognitive decline.

    ...This all came rushing back to me this week when Myriad Genetics, Inc., reported that a Phase 3 clinical trial (the last one before a company seeks FDA approval for a new drug) it had been testing for an experimental Alzheimer's drug had failed. The drug, Flurizan, is called a "selective amyloid lowering agent," or SALA. Amyloid is a peptide (part of a protein). The amyloid known as Aβ42 is--according to the dogma--the "primary initiator of neurotoxicity and amyloid plaque development in the brains of Alzheimer's disease patients," as Myriad puts it. And indeed, in human cells growing in lab dishes as well as in lab animals, Flurizan reduces levels of Aβ42.

    But when Myriad gave it to people with early-stage Alzheimer's, it didn't help them a bit. We don't know why. Maybe Flurizan did not reduce Aβ42 in the patients. Or maybe--and this would be disastrous for the field--it did reduce Aβ42 but that had no beneficial effect. If the latter, it is more proof that the amyloid dogma--Aβ42 causes Alzheimer's, therefore get rid of Aβ42 and you'll cure the disease--is wrong. I call it "disastrous" because a huge majority of the research and drug-development efforts in Alzheimer's assumes that Aβ42 causes the disease and that getting rid of Aβ42 is the holy grail. ...

    ...I'm afraid that's still where things stand, four years after I wrote that. Now let me share a note I just got from a scientist who has long questioned the amyloid dogma:

    "I couldn't resist contacting you....not with glee [about the Myriad failure], instead sadness at how scientific narcissism [he means the focus on the amyloid hypothesis to the near-exclusion of everything else] fails every damn time. . . . As far as Flurizan is concerned, I am sure the amyloid contingent will make their excuses: blame the drug, the placebo group (for not falling fast enough!), the timing (clearly we need to start anti-amyloid therapy in utero!) and, ultimately, the species (humans simply are not as good responders as mice). However, at this stage, I sense that the heads are beginning to drop and the swagger has disappeared. . . . While my hope is that this will open the field to all manner of crazy hypotheses, my fear is that the excuses will be persuasive enough. At this point, everything that lowers amyloid in mice/cells has failed in human trials. Perhaps a coincidence? Maybe. However, the alternate is never really considered. All of this is not to say that I was right [that amyloid is not the cause of Alzheimer's and therefore cannot be the target of drugs to treat it]. I still don't know exactly how amyloid fits into the puzzle. But betting the house on 00 in roulette is no way to conduct science. Trouble is, we mostly are not gambling with our own money or lives." ...

    The comments on the Newsweek blog above are as interesting as the article:

    "Thank you for not being afraid to "suggest" some scandal here. I have been "fighting" a long fight, 4 months! You say that's not long...well it IS in the life of an Alzheimer's patient that you care for and love that is declining every single day -- or WAS declining! ...
    ...There is a treatment that works(perispinal etanercept) and the doctor behind it (Dr. Ed Tobinick)has been pushed into a corner for over 4 years now. They (the experts and professionals) have slandered his name and his treatment, making it almost impossible to get the word out...Almost. But, in the last couple of months, we are finally getting the word out through his persistance and through the persistance of caregivers like me who know this is real, and can't stand the fact that the Pharma companies are shutting this out. Amgen makes the drug, yet they won't stand behind it either. ...Amgen refused to do a study ($$$) and Dr. Tobinick didn't have the kind of funds it takes to do a double-blind clinical trial...so there it sat. But, Dr. Tobinick kept treating patients, and kept plublishing his work in peer-reviewed journals. A couple of weeks ago, a research team at the NIA/NIH finally completed a study that proved it to be Plausible, to be presented at ICAD this month -- Sorry Amgen!!

    Title: Modification of synaptic plasticity by TNF and sphingomyelinase: Implications for cognitive impairment in AD
    Category: Molecular Mechanisms of Neurodegeneration Synpatic disruption
    Author(s): Yue Wang, NIA/NIH, Baltimore, MD, USA. Contact e-mail: wangyu@grc.nia.nih.gov
    Conclusions:
    Our findings reveal rapid, nSmase-mediated, effects of TNF on the function of two types of glutamate receptors that regulate hippocampal synaptic plasticity, and provide a potential explanation for the recently reported rapid improvement in cognitive function of AD patients treated with a TNF inhibitor (Tobnick and Gross, J Neuroinflammation 2008 Jan 9;5:2).

    -------
    ...Please read the following message board for many answers, pros and cons from caregivers regarding this treatment -- And spread the word. It's really long now, so just start at the end and go back a little at a time.
    Link
    There are also a couple of videos up on youtube that us caregivers put up:
    LINK,
    LINK,
    LINK,
    LINK (and more by Bob & Linda)
    With Hope, Felicia McColl


    Posted by Evax (July 3, 2008 at 2:56 )

    The Abeta vaccine targeting Abeta has reduced the burden of amyloid plaques in the brain for both mice and humans, and improved or slowed down deterioration of cognition. When one drug targeting Abeta works whereas another doesn't, blame the drug not the target.

     

    Enbrel, Alzheimer's And A Controversial Doctor

    By Ed Silverman // July 1st, 2008

    "Earlier this year, Amgen went out of its way to disavow a widely publicized case study that suggested Enbrel, which is only approved for treating rheumatoid arthritis and psoriasis, may be useful in combating Alzheimer's disease.
    In fact, the biotech issued successive press releases due to the single-patient case study, which was published last January by a Los Angeles physician in The Journal of Neuroinflammation and that suggested "rapid cognitive improvement" occurred in an 81-year-old patient, beginning only two hours after Enbrel was administered. The case report then noted his improvement lasted during a seven-week follow-up program that included weekly injections...

    ...a statement issued in January was followed by a longer and more emphatic statement this past April, in which Amgen declared it did not "support or endorse" the use of Enbrel for treating Alzheimer's. Moreover, Amgen argued there is "insufficient and unsubstantiated scientific data to support" using Enbrel for this purpose...The biotech also questioned the lack of "placebo-controlled data," and noted the physician's research was never published in a peer-reviewed medical journal. "Anecdotes," Amgen charged, "are not sufficient scientific evidence."

    What follows is a detailed account of Tobinick's history with the drug Enbrel and Amgen, and a very lively discussion in the comments on Tobinick. Well worth reading, although you may be left wondering if the treatment works despite the questionable methods of the doctor involved.

    And back to the Amyloid hypothesis:

    Exonhit says EHT 0202 could be 'major therapeutic breakthrough' in Alzheimer's 07.02.08, 6:10 AM ET

    PARIS (Thomson Financial) - ExonHit Therapeutics' EHT 0202 compound could be a 'major therapeutic breakthrough' in the treatment of Alzheimer's disease, the company said.

    In a preview of a presentation to be given at the International Conference on Alzheimer's Disease in Chicago from July 26 to 31, ExonHit said it is developing two proprietary programmes in Alzheimer's disease.

    EHT 0202, currently in phase II of clinical trials, is based on a mechanism to redirect the processing of APP (Amyloid Precursor Protein), which is pivotal in the evolution of Alzheimer's disease, the company said.

    The second programme, EHT 206, is in pre-clinical stage and focuses on the development of chemical entities aiming at inhibiting the formation of senile plaques, largely composed of aggregated beta amyloid peptides, the company said.
    These plaques play a major role in the loss of cognitive functions in patients suffering from Alzheimer's disease, it said.
    The company is also conducting several studies for a potential blood-based Alzheimer's disease test as part of the EHTDx21 project. These aim to confirm the ability of the test to isolate Alzheimer patients from healthy individuals who show no signs of dementia and to measure the ability of the test to differentiate Alzheimer's from other forms of dementia...

    New Drug Reverses Alzheimer's Disease Within Days In Mouse Models

    ScienceDaily (July 10, 2008) -- Scientists report a remarkable improvement in Alzheimer's transgenic mice following treatment with a new drug. The study provides the first demonstration that an ionophore, a compound that transports metal ions across cell membranes, can elicit rapid and pronounced improvement in neuropathology and cognitive function in mouse models of Alzheimer's Disease (AD).

    Recent research has implicated dysregulation of metal ions in the brain, particularly copper and zinc, in the pathogenesis of AD and the damaging accumulation of amyloid beta (Aβ) protein that is characteristic of this devastating disease. The ionophore clioquinol (CQ), an 8-hydroxyquinoline, has been shown to increase intracellular copper and zinc levels and decrease Aβ levels in cultured cells and in the brains of transgenic (Tg) AD mice. However, further studies in mice and humans demonstrated that brain entry of CQ was quite limited.

    This research is published by Cell Press in the July 10th issue of the journal Neuron.

    Dr. Ashley I. Bush from the Mental Health Research Institute of Victoria in Australia, with Dr. Paul A. Adlard and colleagues examined the therapeutic potential of PBT2, a second generation 8-hydroxyquinoline designed for easier synthesis, higher solubility and increased blood-brain barrier permeability, in two well established Tg mouse models of AD. The Tg mice examined in the study overexpress the precursor protein for Aβ and possess mutations that cause AD in humans. One of the Tg models also expresses the human presenilin deletion mutation that also causes AD.

    "Both types of Tg mice exhibit progressive spatial learning deficits that are accompanied by increasing Aβ levels and plaque formation. Demonstrating benefits of PBT2 treatment in the two separate models was both a stringency test, increasing confidence that PBT2 is more likely to show benefit in clinical trials, and also allowed us to determine whether specific forms of Aβ change in register with cognitive improvement in both strains. This is significant as cognitive loss in AD is not just a simple product of rising Aβ levels," explains Dr. Bush.

    PBT2 was shown to be a superior ionophore when compared to CQ and the researchers went on to test Aβ levels and cognitive outcomes after oral treatment with PBT2. "We found that oral treatment with PBT2 induced a dramatic improvement in learning and memory in both Tg models of AD, accompanied by a marked inhibition of AD-like neuropathology. These outcomes were rapid, with reduction of soluble interstitial Aβ occurring within hours, and significant cognitive benefits seen within days of first administration of the compound," says Dr. Bush.

    These results encourage further testing of compounds that target synaptic metals as a possible treatment of AD. Further, recent clinical trials in AD patients taking oral PBT2 have been promising and support PBT2 as a viable treatment for AD.

    Useful definition for the following article:

    Autophagy (Wikipedia)
    In cell biology, autophagy, or autophagocytosis, is a catabolic process involving the degradation of a cell's own components through the lysosomal machinery. It is a tightly-regulated process that plays a normal part in cell growth, development, and homeostasis, helping to maintain a balance between the synthesis, degradation, and subsequent recycling of cellular products. It is a major mechanism by which a starving cell reallocates nutrients from unnecessary processes to more-essential processes.

    A variety of autophagic processes exist, all having in common the degradation of intracellular components via the lysosome. The most well-known mechanism of autophagy involves the formation of a membrane around a targeted region of the cell, separating the contents from the rest of the cytoplasm. The resultant vesicle then fuses with a lysosome and subsequently degrades the contents.
    It was first described in the 1960s,[1] but many questions about the actual processes and mechanisms involved still remain to be elucidated. Its role in disease is not well categorised; it may help to halt the progression of some diseases and play a protective role against infection by intracellular pathogens; however, in some situations, it may actually contribute to the development of a disease.

    from: Herpes simplex virus type 1 and Alzheimer's disease: The autophagy connection

    DOI: 10.1080/13550280701802543

    Authors: Ruth F. Itzhaki a; S Louise Cosby b; Matthew A. Wozniak a

    Published in: Journal of Neurovirology, Volume 14, Issue 1 January 2008 , pages 1 - 4

    "...Following the authors' previous studies implicating herpes simplex virus type 1 (HSV1) in brain of APOE-ε 4 carriers as a major cause of AD, the authors propose here, on the basis of their and others' recent studies, that not only does HSV1 generate the main components of amyloid plaques and neurofibrillary tangles (NFTs)--β -amyloid (Aβ) and abnormally phosphorylated tau but also, by disrupting autophagy, it prevents degradation of these aberrant proteins, leading to their accumulation and deposition, and eventually to AD.

    It has recently been realised that autophagy is an essential process for maintaining homeostasis and that a decrease in efficiency of autophagy occurs during aging, resulting in the accumulation of undigested products inside lysosomes (Cuervo et al, 2005; Ward, 2002). A role for autophagy in several neurodegenerative diseases has been proposed also, mainly because a defect in autophagy might account for the continuous residence of aberrant proteins in the brain in these diseases and because mice in which basal autophagy in neural cells has been suppressed (by deletion of auto-phagyrelated gene [atg] 5 or 7) suffer neurodegenerative disease, with an accumulation of inclusion bodies and intracellular protein aggregates in brain (Hara et al, 2006; Komatsu et al, 2006). In the case of AD, the relevant proteins--β -amyloid (Aβ) and abnormally phosphorylated tau--are generally thought to be the major culprits in the neurodegenerative process of the disease, although their precise involvement is still unknown; in fact, they are considered by some to be protective, entombing possible damaging agents. The exact nature of the defect in autophagy or the cause of its disruption is unknown. But in Alzhemier's disease (AD) brain, autophagosomes and AVs accumulate in dystrophic neurites (Nixon et al, 2005) and amyloid precursor protein (APP), Aβ, and the enzymes responsible for Aβ formation are present in AVs (Yu et al, 2004).

    Hypothesis

    We propose the following scenario: HSV1 enters the brain in older age, as the immune system declines, either from the peripheral nervous system (PNS) where, after infection earlier in life, it has resided latently, or as a new infection via the olfactory route. The virus becomes latent in the brain but reactivates periodically under conditions of immunosuppression or stress--e.g., during systemic infection. The reactivated virus then causes limited local damage, i.e., an atypical type of HSE [Herpes Simplex Encephalitis] (a number of cases of "mild" and recurrent HSE have been reported (Fodor et al, 1998; Klapper et al, 1984)). The damage occurs probably through direct viral action and also indirectly, via inflammatory/oxidative effects, thereby augmenting any such processes if already occurring, and these processes lead to deposition of Aβ and to AD-like phosphorylation of tau. Defective autophagy--a consequence of aging--is exacerbated by viral action via the ICP34.5 gene and this prevents not only degradation of the HSV1 but also degradation of the aberrant cell proteins, so that they remain as permanent residents in the brain. Subsequent deposition of other materials on the Aβ and abnormal tau leads to formation respectively of amyloid plaques and neurofibrillary tangles.


    from: Calcium May Be The Key To Understanding Alzheimer's Disease

    ScienceDaily (July 17, 2008) -- Researchers at the University of Pennsylvania School of Medicine have shown that mutations in two proteins associated with familial Alzheimer's disease disrupt the flow of calcium ions within neurons. The two proteins, called PS1 and PS2 (presenilin 1 and 2), interact with a calcium release channel in an intracellular cell compartment.

    "The 'calcium dysregulation' hypothesis for inherited, early onset familial Alzheimer's disease has been suggested by previous research findings, but our current study identifies a molecular mechanism that makes this hypothesis very compelling," says lead author J. Kevin Foskett, PhD, Professor of Physiology.

    "Mutated PS1 and PS2 caused exaggerated cellular calcium signaling in cells through a calcium channel in the endoplasmic reticulum called the inositol trisphosphate receptor [InsP3R], suggesting that it or other proteins in this calcium signaling pathway could be targets for new Alzheimer's disease therapies."

    The study appeared in the June 26 issue of Neuron.

    Alzheimer's disease affects as many as 5 million Americans, 5 percent of whom have the familial form. The hallmark of the disease is the accumulation of tangles and plaques of amyloid beta protein in the brain. "The amyloid hypothesis has long been invoked to explain the cause of Alzheimer's" says Foskett. In the Neuron study, cells that carried the disease-causing mutated form of PS1 showed increased processing of amyloid beta that depended on the interaction of the PS proteins with the InsP3R. This observation links mis-regulation of calcium inside cells with the production of amyloid, a characteristic feature in the brains of people with Alzheimer's disease.

    ...These new observations suggest that new approaches could be explored. The next steps are to find out if other mutations in PS1 and PS2 that cause Alzheimer's disease have a similar effect on calcium signaling in the brain, and to identify drugs that might inhibit the interaction between InsP3R and PS1 or PS2 specifically in the brain.

    "The significance of identifying the molecular mechanism and pathway of disrupted calcium signaling is that a number of novel treatment targets can now be developed and tested," says Foskett.

    from: Brain 'trick' offers treatment hope for Alzheimer's

    Scientists in the UK and Canada have made a significant step forward in the search for new drugs to treat Alzheimer's disease. One of the causes of neurodegeneration is a modification to the protein 'tau', which helps to maintain the stability of neurones in the brain, causing them to form aggregates termed 'tangles'. These diseases, or 'tauopathies' are believed to be caused by a form of the protein tau which has been excessively modified with phosphate. By studying the chemistry and structure of relevant enzymes, the research teams at York, led by Professor Gideon Davies, and Simon Fraser, led by Professor David Vocadlo, have designed an enzyme inhibitor that prevents the phosphorylation of tau in animal models. They have effectively tricked the brain's own enzymes into installing a sugar on to tau in place of the detrimental phosphates. The enzyme inhibitor, termed a 'thiazoline', developed by Professor Vocadlo and Professor Davies is not yet a drug, but it is a major breakthrough in finding compounds that cross the blood-brain barrier to elicit beneficial effects that prevent the onset of tauopathies...

    from: Alzheimer's Research Brings Progress, Setbacks
    By Steven Reinberg
    HealthDay Reporter
    Friday, July 18, 2008; 12:00 AM

    FRIDAY, July 18 (HealthDay News) -- It's one step forward, one step back in the search for treatments against Alzheimer's disease.

    In one of two studies in the July 19 issue ofThe Lancet, an older drug called dimebon significantly improved Alzheimer's symptoms. But in a second report, a once-promising vaccine failed to prevent the progression of Alzheimer's -- even though it cleared dementia-linked amyloid plaques in the brain.

    ...In one study, British researchers led by Dr. Clive Holmes, from the Memory Assessment and Research Centre at Moorgreen Hospital in Southampton, analyzed data on 80 Alzheimer's patients who were treated with an experimental vaccine that for now is dubbed AN1792...

    Indeed, long-term follow-up of Alzheimer's patients treated with AN1792 did show, "a reduction in the number of plaques in the brains of patients -- in some cases there was a virtually complete removal of plaques," Holmes said.

    But there was a catch. "Crucially, there was no evidence that the patients benefited by the removal of plaques and even those subjects with virtually complete removal continued to deteriorate and had severe end-stage dementia prior to their death," Holmes said.

    ...Dr. Sam Gandy, chairman of the Alzheimer's Association's National Medical and Scientific Advisory Council, said the new finding suggests that other forces besides plaque build-up are driving disease progression.

    "If you don't start with your vaccine until you are at a later stage of disease and other processes are already established, the horse may be already out of the barn," Gandy said. "It is possible that amyloid is like a match lighting a fire and once the fire is out of control, dealing with the match isn't that effective."

    But there was better news in a second study. In that work, Dr. Rachelle S. Doody, a professor of neurology at the Alzheimer's Disease and Memory Disorders Center at Baylor College of Medicine in Houston, and her colleagues studied the effects of the drug dimebon on 183 patients in Russia with mild to moderate Alzheimer's disease. The drug is currently not marketed anywhere, and was previously used in Russia as an antihistamine...

    ..After six months, Doody's team found that patients on dimebon had significant improvement in cognitive ability, compared with those receiving placebo.

    "We found treated patients were improved in their thinking abilities, their behavioral symptoms [and] their daily skills abilities, compared to people who took placebo," she said....

    ...At six months, patients receiving dimebon showed an improvement of 1.9 points on the ADAS-cog scale from the beginning of the study, while those on placebo continued to decline. After a year, those receiving dimebon showed a 6.9 point increase on the ADAS-cog scale, the researchers report.

    "This first trial was promising," Doody said. "This is not a cure for Alzheimer's disease, but the benefits could last for a long time. The drug appears to slow the clinical progression of the disease."...

    ...Another phase III trial has just started, Doody said. This six-month trial is being conducted in the United States, Europe and South America and is now in the process of recruiting several hundred patients, she noted.

    More a comment on the National Health Service in the UK than research:

    from: Woman stole thousands to pay for grandmother's Alzheimer drug, court told
    By Kate Devlin, Medical Correspondent
    Last Updated: 8:42PM BST 03/07/2008

    Fiona Bartlett, 41, stole the cash from her employer so she could buy the drug Aricept, which can slow down the progress of the disease. Using false identities she authorised a total of 18 loans for herself with Provident Personal Credit....At the time she was paying around £250 a month for the medication, which, on top of private consultation fees, left her with debts of £20,000....

    Her grandmother, who is in her 90s, had previously received Aricept when she lived in Kent. But when she moved to Basingstoke, Hants, to be cared for by her granddaughter, she was no longer able to get the drug on the NHS... She told her employers what she had done when she could no longer keep up with the repayments.

    Nicholas Bates, defending, said that the crimes had not been committed so that his client could enjoy a "champagne lifestyle", and that the money was used solely to fund her grandmother's treatment. He added that she had already started to repay the money to her employer.

    Prosecutor Linda Jones told the court that Bartlett, who worked as an agent for the firm, had a previous conviction for a similar breach of trust. Bartlett admitted six counts of submitting false loan applications to Provident Personal Credit, for a total of £2,050...

    Speaking outside court, she said: "What I did was awful, but what do you do when you know something works?

    "Without Aricept my grandmother was terrified - she was like a toddler who was being attacked."

    The Alzheimer's Society believes that the £2.50 a day drug should be available on the NHS to sufferers at all stages of the illness.

    However, in 2005 the National Institute for Clinical Excellence (Nice), the government's drugs watchdog, recommended that it should only be prescribed to patients with "moderate" Alzheimer's, meaning that thousands of patients have to wait until their disease has progressed before they can access the treatment.

    Hampshire Primary Care Trust said its policy is to follow the Nice guidelines and decisions about prescribing the medication lie with consultants....Martin Robinson, director of operations for older people's mental health services at Hampshire Partnership NHS Trust, said: "We prescribe memory drugs in line with NICE guidance and this includes Aricept, Reminyl and Exelon...Nice says that providing the drug to all Alzheimer's patients, of which there are around 400,000 in Britain, would be too expensive.

     

    References:

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