Alzheimer Disease: Vellas B

Vellas B, Gauthier S, Allain H, Andrieu S, Aquino JP, Berrut G, Berthel M, Blanchard F, Camus V, Dartigues JF, Dubois B, Forette F, Franco A, Gonthier R, Grand A, Hervy MP, Jeandel C, Joel ME, Jouanny P, Lebert F, Michot P, Montastruc JL, Nourhashemi F, Ousset PJ, Pariente J, Rigaud AS, Robert P, Ruault G, Strubel D, Touchon J, Verny M, Vetel JM, Anonymous00344. · CHU Casselardit, Toulouse. · Rev Neurol (Paris). · Pubmed #16244574 No free full text.

Abstract: Under the auspices of the French Society of Gerontology and Geriatrics, a multidisciplinary team including geriatritians, neurologists, epidemiologists, psychiatrists, pharmacologists and public health specialists developed a consensus on care for patients with severe dementia. They defined 21 recommendations for general practitioners, long-term care physicians and specialists based on knowledge available in 2005. At all stages of the disease, the objective of care is to improve as much as possible quality-of-life for the patient and his/her family, including a life project until the end of life. It is always possible to do something for these patients and their family: nutritional status, behavior disorders, and incapacities to deal with basic activities of daily life have to be taken in consideration. Resource allocation and proximity care have to be targeted. Research areas necessary to improve the care of patients with severe dementia has been selected.

Nourhashémi F, Vellas B. · No affiliation provided · Expert Rev Neurother. · Pubmed #18457525 No free full text.

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Vellas B, Anonymous00051. · No affiliation provided · J Nutr Health Aging. · Pubmed #16554942 No free full text.

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Vellas B. · No affiliation provided · Rev Med Interne. · Pubmed #14710443 No free full text.

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Andrieu S, Reynish W, Vellas B. · No affiliation provided · J Nutr Health Aging. · Pubmed #11135799 No free full text.

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Voisin T, Vellas B. · INSERM U825, Alzheimer's Disease Research Centre (CMRR); F-CMRR-SF, Toulouse University Hospital, Toulouse, France. · Drugs Aging. · Pubmed #19220070 No free full text.

Abstract: In contrast with the earlier stages and, in particular, the predementia stage, of Alzheimer's disease (AD), severe dementia is often neglected. However, the advanced stages of dementia are just as important as the earlier stages because of their frequency, their impact on the lives of patients and their caregivers, and their economic consequences. All patients with moderately severe to severe dementia must be evaluated for cognitive, functional, psychological and behavioural symptoms. Thorough and regular evaluation of patients in the advanced stages of the disease has the following objectives: improving patients' quality of life by encouraging use of their remaining capacities; setting up or modifying a care plan; playing a role in the follow-up of measures instituted; and documenting the natural history of the disease. Therapeutic trials with cholinesterase inhibitors and memantine have been conducted in patients with severe stages of AD. As a consequence, memantine has been approved by numerous drug agencies and donepezil has been approved by the US FDA for use in severe stages of the disease. However, it is important to note that at this stage of AD, and perhaps more than in any other, management must be global and multidisciplinary because of the expression of the disease, its complications and intercurrent disorders. Indeed, thorough knowledge by health professionals of the expression of all disease disorders and intercurrent disorders, and of their significance during the severe stage of AD, is important in the management of these patients to limit complications and facilitate prompt establishment of appropriate care. More effort is needed in both clinical and research settings to ensure that patients with severe AD and their relatives can be offered optimal management.

Vellas B, Coley N, Andrieu S. · Gerontopole, CHU Toulouse, Department of Geriatric Medicine, Toulouse, France. · J Alzheimers Dis. · Pubmed #18953115 No free full text.

Abstract: Disease modifying trials are becoming increasingly common in the field of Alzheimer's disease (AD) as the search for a treatment able to slow the progression of this disease continues. In this paper, we briefly discuss the methodological considerations for disease modifying trials that were addressed during three recent international task force meetings involving specialists in the field of AD trials. Topics covered included study design, the identification of appropriate outcomes, the use of biomarkers, and the identification of suitable study populations. We also provide an update on recent disease modifying trials which have enabled us to gain experience in the use of biomarkers and have helped to define suitable outcomes, and consider how they can help us to shape future perspectives for disease modifying trials.

Gillette-Guyonnet S, Vellas B. · Gérontopôle Toulouse, France. · Curr Opin Clin Nutr Metab Care. · Pubmed #18827571 No free full text.

Abstract: PURPOSE OF REVIEW: In addition to extending lifespan, animal research shows that specific diets benefit brain functioning. Indeed, it has been proven that caloric restriction prevents age-related neuronal damage. What are those mechanisms involved in the effects of caloric restriction on brain functioning? Could caloric restriction be proposed in the future to prevent or treat neurodegenerative disorders such as Alzheimer's disease? Is there a future for caloric restriction interventions in adults? RECENT FINDINGS: Hypotheses linking caloric restriction to cognitive capability include anti-inflammatory mechanisms, reduction of neural oxidative stress, promotion of synaptic plasticity, induction of various stress and neurotrophic/neuroprotective factors. Caloric restriction may also prevent beta-amyloid neuropathology in Alzheimer transgenic models. Finally, both exercise and caloric restriction enhance neurogenesis via different mechanisms suggesting that their combination may decrease the risk of neurodegenerative disease. SUMMARY: It is now well established that caloric restriction could be used to promote successful brain aging. Data from randomized controlled trials in humans are limited. No positive effect on cognitive impairment was found probably due to methodological limitations. The long-term effects of caloric restriction in adults must be clarified before engaging in such preventive strategy. Additional animal studies must be conducted in the future to test the effects of 'multidomain' interventions (caloric restriction plus regular exercise) on age-related cognitive decline.

Coley N, Andrieu S, Gardette V, Gillette-Guyonnet S, Sanz C, Vellas B, Grand A. · INSERM Unit 558, Toulouse, France. · Epidemiol Rev. · Pubmed #18779228 No free full text.

Abstract: The prevention of neurodegenerative dementias, such as Alzheimer disease, is a growing public health concern, because of a lack of effective curative treatment options and a rising global prevalence. Various potential risk or preventive factors have been suggested by epidemiologic research, including modifiable lifestyle factors, such as social contacts, leisure activities, physical exercise, and diet, as well as some preventive pharmacologic strategies, such as hormone replacement therapy, nonsteroidal antiinflammatory drugs, and Ginkgo biloba. Some factors have been targeted by interventions tested in randomized controlled trials, but many of the results are in conflict with observational evidence. The aim of this paper is to review the epidemiologic data linking potential protective factors to dementia or cognitive decline and to discuss the methodological limitations that could explain conflicting results. A thorough review of the literature suggests that, even if there are consistent findings from large observational studies regarding preventive or risk factors for dementia, few randomized controlled trials have been designed specifically to prove the protective effects of interventions based on such factors on dementia incidence. Because of the multifactorial origin of dementia, it appears that multidomain interventions could be a suitable candidate for preventive interventions, but designing such trials remains very challenging for researchers.

Villars H, Gillioz AS, Hein C, Voisin T, Nourhashemi F, Soto ME, Arbus C, Ousset PJ, Vellas B. · Service de médecine interne gériatrique et gérontologie clinique, Gérontopôle, CHU Toulouse, Hôpital Purpan Casselardit, Toulouse. · Rev Neurol (Paris). · Pubmed #18680826 No free full text.

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Rolland Y, Abellan van Kan G, Vellas B. · Inserm, Toulouse, France; University of Toulouse III, Toulouse, France. · J Am Med Dir Assoc. · Pubmed #18585641 No free full text.

Abstract: A number of factors, including physical activity, may contribute to prevention of cognitive decline and delay the onset of dementia. In addition to its convincing multiple benefits, an increasing body of evidence suggests that an active life has a protective effect on brain functioning in elders. Physical activity may also slow down the course of Alzheimer's disease. These hypotheses have led to increasing research in this specific area during the past decade. This review systematically analyzes the current literature on Alzheimer's disease and the effect of physical activity. Epidemiological studies, short-term randomized controlled trials (RCTs) in nondemented participants, and biological research suggest that physical activity improves cognitive function in older subjects. The limitations of these works are discussed. No RCTs have yet demonstrated that regular physical activity prevents dementia. Additional challenging clinical interventional studies are needed to demonstrate this relationship, but accumulating evidence from biological research is available. Defining the optimal preventive and therapeutic strategies in terms of type, duration, and intensity of physical activity remain an open question. In the future, the prevention of Alzheimer's disease may be based on rules governing lifestyle habits such as diet, cognitive activity, and physical activity.

Vellas B, Andrieu S, Sampaio C, Coley N, Wilcock G, Anonymous00158. · Inserm U558, Toulouse, France. · Lancet Neurol. · Pubmed #18420157 No free full text.

Abstract: Harmful consequences in health status caused by disease are referred to as outcomes, and in clinical studies the measures of these outcomes are called endpoints. A major challenge when deciding on endpoints is to represent the outcomes of interest accurately, and the accuracy of such representation is assessed through validation. Complex diseases like Alzheimer's disease have many different and interdependent outcomes. We present a consensus for endpoints to be used in clinical trials in Alzheimer's disease, agreed by a European task force under the auspices of the European Alzheimer Disease Consortium. We suggest suitable endpoints for primary and secondary prevention trials, for symptomatic and disease-modifying trials in very early, mild, and moderate Alzheimer's disease, and for trials in severe Alzheimer's disease. A clear and consensual definition of endpoints is crucial for the success of further clinical trials in the field and will allow comparison of data across studies.

Aalten P, Verhey FR, Boziki M, Brugnolo A, Bullock R, Byrne EJ, Camus V, Caputo M, Collins D, De Deyn PP, Elina K, Frisoni G, Holmes C, Hurt C, Marriott A, Mecocci P, Nobili F, Ousset PJ, Reynish E, Salmon E, Tsolaki M, Vellas B, Robert PH. · Department of Psychiatry and Neuropsychology, Alzheimer Centre Limburg, Maastricht University Hospital, Maastricht, The Netherlands. · Dement Geriatr Cogn Disord. · Pubmed #18025783 links to  free full text

Abstract: BACKGROUND/AIMS: The aim of this study was to determine the consistency of neuropsychiatric subsyndromes of the Neuropsychiatric Inventory across several clinical and demographic subgroups (e.g. dementia subtypes, dementia severity, medication use, age and gender) in a large sample of outpatients with dementia. METHODS: Cross-sectional data of 2,808 patients with dementia from 12 centres from the European Alzheimer's Disease Consortium were collected. Principal component analysis was used for factor analysis. Subanalyses were performed for dementia subtypes, dementia severity, medication use, age and gender. RESULTS: The results showed the relatively consistent presence of the 4 neuropsychiatric subsyndromes 'hyperactivity', 'psychosis', 'affective symptoms' and 'apathy' across the subanalyses. The factor structure was not dependent on dementia subtypes, age and gender but was dependent on dementia severity and cholinesterase use. The factors hyperactivity and affective symptoms were present in all subanalyses, but the presence of the factors apathy and psychosis was dependent on use of cholinesterase inhibitors and dementia severity, respectively. CONCLUSION: The present study provided evidence of the relative consistency of neuropsychiatric subsyndromes across dementia subtypes, age and gender, thereby stressing the importance of thinking about neuropsychiatric subsyndromes instead of separate symptoms. However, the subsyndromes apathy and psychosis were dependent on use of cholinesterase inhibitors and dementia severity.

Aalten P, Verhey FR, Boziki M, Bullock R, Byrne EJ, Camus V, Caputo M, Collins D, De Deyn PP, Elina K, Frisoni G, Girtler N, Holmes C, Hurt C, Marriott A, Mecocci P, Nobili F, Ousset PJ, Reynish E, Salmon E, Tsolaki M, Vellas B, Robert PH. · Department of Psychiatry and Neuropsychology, Alzheimer Centre Limburg, Maastricht University Hospital, Maastricht, The Netherlands. · Dement Geriatr Cogn Disord. · Pubmed #17986816 links to  free full text

Abstract: BACKGROUND/AIMS: The aim of this study was to identify neuropsychiatric subsyndromes of the Neuropsychiatric Inventory in a large sample of outpatients with Alzheimer's disease (AD). METHODS: Cross-sectional data of 2,354 patients with AD from 12 centres from the European Alzheimer's Disease Consortium were collected. Principal component analysis was used for factor analysis. RESULTS: The results showed the presence of 4 neuropsychiatric subsyndromes: hyperactivity, psychosis, affective symptoms and apathy. The subsyndrome apathy was the most common, occurring in almost 65% of the patients. CONCLUSION: This large study has provided additional robust evidence for the existence of neuropsychiatric subsyndromes in AD.

Aisen PS, Gauthier S, Vellas B, Briand R, Saumier D, Laurin J, Garceau D. · Department of Neurology, Georgetown University, Washington, DC 20057, USA. · Curr Alzheimer Res. · Pubmed #17908052 No free full text.

Abstract: As a potential disease-modifying treatment for AD, Alzhemed (tramiprosate) is a compound that binds to soluble amyloid-beta peptide (Abeta) and inhibits the formation of neurotoxic aggregates that lead to amyloid plaque deposition in the brain. The safety, tolerability, and pharmacodynamic effects of Alzhemed were assessed in a double-blind study in which 58 individuals with mild-to-moderate AD (MMSE 13-25) were randomized to receive placebo or Alzhemed 50, 100 or 150 mg BID for 3 months. At the end of the double-blind phase, 42 of these subjects entered a 36-month open-label (OL) phase in which they received Alzhemed 150 mg BID. Assessments included plasma and cerebrospinal fluid (CSF) Alzhemed concentrations, CSF levels of Abeta, as well as cognitive (Alzheimer's Disease Assessment Scale-cognitive subscale, Mini-Mental State Examination) and clinical performance (Clinical Dementia Rating scale, Sum-of-Boxes) measures. Alzhemed was safe and well tolerated, crossed the blood-brain barrier, and dose-dependently reduced CSF Abeta(42) levels after 3 months of treatment. Mild AD subjects (MMSE 19-25 at entry) displayed greater reduction of CSF Abeta(42) levels than moderate AD participants (MMSE 13-18 at entry). There was no effect of Alzhemed on the cognitive or clinical measures after 3 months of treatment. The OL follow-up suggested a stabilization of cognitive function especially in mild AD subjects over the 36-month study period. Alzhemed thus appears to be well tolerated with long-term exposure and reduces CSF Abeta(42) levels in mild-to-moderate AD subjects. These findings will be discussed in the context of two large-scale randomized, double-blind, placebo-controlled Phase III clinical trials that are currently being conducted to test the long-term safety and efficacy of Alzhemed.

Cortes F, Portet F, Touchon J, Vellas B. · F. Cortes, Alzheimer's Disease Research Centre, U 558, Toulouse, France. · J Nutr Health Aging. · Pubmed #17653493 No free full text.

Abstract: BACKGROUND: Clinical trials in Alzheimer's disease (AD) include patients benefiting from recent improvements in AD management. OBJECTIVE: To observe the progression of Alzheimer's disease (AD) after 6 and 18 months in patients treated with acetylcholinesterase inhibitors (AChEI) in order to determine the best duration of follow-up necessary to demonstrate the impact of new drugs. METHODS: Six hundred and eleven patients included in the REAL.FR cohort were treated with AChEI at baseline. We describe the cognitive, functional, behavioural, nutritional and global changes in the 509 and 364 patients who completed 6 and 18 months of follow-up, respectively, and who did not discontinue treatment. RESULTS: After 6 and 18 months, we observed a statistically significant change in the MMSE (-0.54 +/- 3.13 at 6 months and -2.90 +/- 4.10 at 18 months), ADAS-cog (1.58 +/- 5.23 and 4.02 +/- 6.83), ADL (-0.30 +/- 0.79 and -0.84 +/- 1.20), IADL (-0.31 +/- 0.95 and -0.94 +/- 1.20), CDR sum of boxes (0.75 +/- 2.03 and 2.65 +/- 3.18) and MNA scores (-0.42 +/- 2.89 and -0.95 +/- 3.57), demonstrating the progression of AD. But on examining these changes, it appears that even if they were statistically significant at 6 months, they do not appear to be clinically relevant or sufficient to allow the observation of the effect of a new drug at this time, whereas such observation would be possible after 18 months. Similar results were obtained in a subgroup of patients who answer to the inclusion criteria of disease modifying trials which confirms the need for having 18 months of follow-up. CONCLUSION: Changes in AD in patients under AChEI treatment are not sufficient to demonstrate the effect of a new treatment at 6 months. However, 18-month trials appear to have the potential to demonstrate clearly the effect of a new drug.

Soto M, Reynish E, Nourhashémi F, Vellas B. · Service de médecine interne et de gérontologie clinique, CHU Purpan-Casselardit, Toulouse (31). · Presse Med. · Pubmed #17560762 No free full text.

Abstract: Alzheimer disease is diagnosed in only half of the patients with this disease in France. In its typical form, it is characterized at the onset by short-term memory problems, repetitive and unusual oversights and forgetfulness, and difficulties in learning new information. Dementia is responsible for more than 50% of the need for care in the elderly. Disease progression is accompanied by noncognitive complications. The 3 most frequent are psychological and behavioral symptoms, weight loss, and impaired balance and walking. Its progressive nature and potential complications underline the need for multidisciplinary management for patients and their families, with regular medical follow-up.

Gillette Guyonnet S, Abellan Van Kan G, Andrieu S, Barberger Gateau P, Berr C, Bonnefoy M, Dartigues JF, de Groot L, Ferry M, Galan P, Hercberg S, Jeandel C, Morris MC, Nourhashemi F, Payette H, Poulain JP, Portet F, Roussel AM, Ritz P, Rolland Y, Vellas B. · Service de Medecine Interne et de Gerontologie Clinique, Pavillon J.P. Junod, Centre Hospitalier Universitaire La Grave-Casselardit, Toulouse cedex 9, France. · J Nutr Health Aging. · Pubmed #17435956 No free full text.

Abstract: Cognitive impairment can be influenced by a number of factors. The potential effect of nutrition has become a topic of increasing scientific and public interest. In particular, there are arguments that nutrients (food and/or supplements) such as vitamins, trace minerals, lipids, can affect the risk of cognitive decline and dementia, especially in frail elderly people at risk of deficiencies. Our objective in this paper is to review data relating diet to risk of cognitive decline and dementia, especially Alzheimer's disease (AD). We chose to focus our statements on homocysteine-related vitamins (B-vitamins), antioxidant nutrients (vitamins E and C, carotenoids, flavonoids, enzymatic cofactors) and dietary lipids. Results of epidemiological studies may sometimes appeared conflicting; however, certain associations are frequently found. High intake of saturated and trans-unsaturated (hydrogenated) fats were positively associated with increased risk of AD, whereas intake of polyunsaturated and monounsaturated fats were protective against cognitive decline in the elderly in prospective studies. Fish consumption has been associated with lower risk of AD in longitudinal cohort studies. Moreover, epidemiologic data suggest a protective role of the B-vitamins, especially vitamins B9 and B12, on cognitive decline and dementia. Finally, the results on antioxidant nutrients may suggest the importance of having a balanced combination of several antioxidant nutrients to exert a significant effect on the prevention of cognitive decline and dementia, while taking into account the potential adverse effects of these nutrients. There is no lack of attractive hypotheses to support research on the relationships between nutrition and cognitive decline. It is important to stress the need to develop further prospective studies of sufficiently long duration, including subjects whose diet is monitored at a sufficiently early stage or at least before disease or cognitive decline exist. Meta analyses should be developed, and on the basis of their results the most appropriate interventional studies can be planned. These studies must control for the greatest number of known confounding factors and take into account the impact of the standard social determinants of food habits, such as the regional cultures, social status, and educational level.

Gillette Guyonnet S, Andrieu S, Vellas B. · Service de Medecine Interne et de Gerontologie Clinique, Pavillon J.P. Junod, Centre Hospitalier Universitaire La Grave-Casselardit, Toulouse cedex 9, France. · J Nutr Health Aging. · Pubmed #17435954 No free full text.

Abstract: Silica present in drinking water may be protective with respect to the decrease of cognitive function as it was suggested by several epidemiologic studies. Data from French cohort have demonstrated that aluminium in drinking water seems to have a deleterious effect and increased the risk of cognitive impairment when the silica concentrations were low. Moreover, it has been shown that the performances to a cognitive test were positively correlated to the consumption of silica and that the risk of Alzheimer's disease (AD) was reduced in subjects who had the higher daily silica intake compared to the others. The silica is probably the natural antidote of the aluminium and could play a benefit role by decreasing the biodisponibility of aluminium, whose neurotoxicity is now clearly established. Data have suggested the possible use of silicates as a therapeutic agent for AD since both model tangles and precipitated beta-pleated sheets of betaA4 can be reversed to soluble forms by silicates. The role of silica in drinking water on cognitive function has been however little studied and clear results have not yet emerge. The potential benefit of silica needs to be confirmed in additional investigations to exclude causes of error related to certain methodological biases. If such association do indeed exist, interventional strategies could be set up to reduce the incidence of AD. The aim of this paper is to review articles published on silica present in drinking water in relation with AD and associated disorders.

Gillette Guyonnet S, Abellan Van Kan G, Alix E, Andrieu S, Belmin J, Berrut G, Bonnefoy M, Brocker P, Constans T, Ferry M, Ghisolfi-Marque A, Girard L, Gonthier R, Guerin O, Hervy MP, Jouanny P, Laurain MC, Lechowski L, Nourhashemi F, Raynaud-Simon A, Ritz P, Roche J, Rolland Y, Salva T, Vellas B, Anonymous00256. · No affiliation provided · J Nutr Health Aging. · Pubmed #17315079 No free full text.

Abstract: Weight loss, together with psychological and behavioural symptoms and problems of mobility, is one of the principal manifestations of Alzheimer's disease (AD). Weight loss may be associated with protein and energy malnutrition leading to severe complications (alteration of the immune system, muscular atrophy, loss of independence). Various explanations have been proposed such as atrophy of the mesial temporal cortex, biological disturbances, or feeding behaviours; however, none has been proven. Prevention of weight loss in AD is a major issue. It requires regular follow-up and must be an integral part of the care plan. The aim of this article is to review the present state of scientific knowledge on weight loss associated with AD. We will consider four points: the natural history of weight loss, its known etiological factors, its consequences and the various management options.

Vellas B, Andrieu S, Sampaio C, Wilcock G, Anonymous00068. · Alzheimer Disease Research and Clinical Center, University of Toulouse, Toulouse, France. · Lancet Neurol. · Pubmed #17166802 No free full text.

Abstract: After symptomatic treatments, the new target for therapeutic approaches in Alzheimer's disease is the development of disease-modifying drugs. The concept of disease modification in Alzheimer's disease is controversial and the design of these trials raises many questions. Which populations should be studied? For how long? With which principal and secondary endpoints? Are surrogate markers available? Here, we present a European consensus on disease-modifying trials in Alzheimer's disease, agreed under the auspices of the European Alzheimer's Disease Consortium and based on the European perspective of the concept of disease modification, study designs, the role for biomarkers, risk benefit, and pharmacoeconomic issues.

Vellas B, Andrieu S, Ousset PJ, Ouzid M, Mathiex-Fortunet H, Anonymous00380. · INSERM (French National Institute of Health and Medical Research), U558, F-31073 Toulouse, France. · Neurology. · Pubmed #17101932 No free full text.

Abstract: BACKGROUND: Preventive approaches in the field of Alzheimer disease (AD) is important but these trials raise many questions. Which protective factor should be studied? What population should be studied? With which principal and secondary criteria? We present here the design of the ongoing GuidAge Study. In the past, several studies suggest that Ginkgo biloba could have a potential benefit effect on cognitive function. The aim of the GuidAge Study is to evaluate the efficacy of 240 mg/d of EGb 761 in the prevention of AD. METHODS: GuidAge is a 5-year double-blind randomized trial conducted in France by a private practice/hospital network of general practitioners and hospital practitioners specializing in memory disorders. This study enrolled elderly subjects with spontaneous memory complaint and the primary outcome is the incidence of AD during a 5 years follow-up period. A total of 2854 subjects were enrolled between March 2002 and September 2004. The age of the study population was 76.8 +/- 4.4 with mean MMSE at entry 27.8 +/- 1.7. CONCLUSION: The GuidAge study is the largest study carried out in Europe on the prevention of AD. Final results should be available in 2010.

Geldmacher DS, Frolich L, Doody RS, Erkinjuntti T, Vellas B, Jones RW, Banerjee S, Lin P, Sano M. · Memory Disorders Program, Department of Neurology, University of Virginia, Box 800394, Charlottesville, Virginia 22908, USA. · J Nutr Health Aging. · Pubmed #17066215 No free full text.

Abstract: Alzheimer's disease (AD) is a progressive degenerative disease that warrants active management to delay or slow progression of its symptoms. The symptoms of AD encompass behavior and daily function as well as cognition, so clinicians should take a global view in the assessment of treatment success. Because there is currently no cure for AD, one cannot expect an initial cognitive improvement observed in the first few months of therapy to be sustained indefinitely. However, one should expect that the patient who is treated early and persistently with medication for AD will show less evidence of behavioral, functional, and cognitive deterioration over a period of time than one would expect in the absence of pharmacotherapy. Thus, treatment success includes not only short-term improvement of symptoms but also less decline over the long term. Determination of treatment success therefore also requires awareness of the typical progression of untreated AD. In this article we review the natural history of AD and evidence for the effectiveness of the treatments indicated for AD: donepezil, galantamine, rivastigmine, and memantine.

Bombois S, Lebert F, Vellas B, Pasquier F. · Centre mémoire de ressource et de recherche, EA 2691, CHRU de Lille, 59037 Lille. · Rev Prat. · Pubmed #16396232 No free full text.

Abstract: Alzheimer's disease (AD) is a neurodegenerative disorder with a decline in memory and cognitive abilities. During the past 20 years, research on AD has increased the knowledge of the physiopathological mechanisms leading to the disease. The major hallmarks of AD are amyloid plaques and neurofibrillary tangles, associated with a prevalent and early cholinergic deficit and an excitotoxicity with inflammation. These pathological mechanisms represent current and future therapeutic targets. cholinesterase inhibitors were the first therapeutic class that has consistently shown a clinical efficacy and safety in patients with mild to moderate ad. more recently glutamate receptor antagonists have been shown effective in the management of patients with moderate to severe AD. These two therapeutic classes could improve cognitive functions, slow the progression of the cognitive decline, prevent some behavioural changes and delay institutionalisation. However, AD represents a problem of public health and preventive and curative strategies have to be proposed.

Vellas B, Gauthier S, Allain H, Andrieu S, Aquino JP, Berrut G, Berthel M, Blanchard F, Camus V, Dartigues JF, Dubois B, Forette F, Franco A, Gonthier R, Grand A, Hervy MP, Jeandel C, Joel ME, Jouanny P, Lebert F, Michot P, Montastruc JL, Nourhashemi F, Ousset PJ, Pariente J, Rigaud AS, Robert P, Ruault G, Strubel D, Touchon J, Verny M, Vetel JM. · No affiliation provided · J Nutr Health Aging. · Pubmed #16222399 No free full text.

This publication has no abstract.