Articulo comentado

Dr. Enrique Arrieta Antón
Médico de Familia. Centro de Salud Segovia Rural (Segovia)
Coordinador del Grupo de Trabajo de Neurología de la SEMERGEN
Comité Científico kNOW Alzheimer
14/10/2014

Barnard ND, Bush AI, Ceccarelli A, Cooper C, De Jager CA, Erickson KI, Fraser G, Kesler S, Levin SM, Lucey B, Morris MC, Squitti R. Dietary and lifestyle guidelines for the prevention of Alzheimer’s disease. Neurobiol Aging. 2014; 35: S74-S78.

Abstract

Risk of developing Alzheimer’s disease is increased by older age, genetic factors, and several medical risk factors. Studies have also suggested that dietary and lifestyle factors may influence risk, raising the possibility that preventive strategies may be effective. This body of research is incomplete. However, because the most scientifically supported lifestyle factors for Alzheimer’s disease are known factors for cardiovascular diseases and diabetes, it is reasonable to provide preliminary guidance to help individuals who wish to reduce their risk. At the International Conference on Nutrition and the Brain, Washington, DC, July 19e20, 2013, speakers were asked to comment on possible guidelines for Alzheimer’s disease prevention, with an aim of developing a set of practical, albeit preliminary, steps to be recommended to members of the public. From this discussion, 7 guidelines emerged related to healthful diet and exercise habits.

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Artículo comentado

Dr. Enrique Arrieta Antón
Médico de Familia. Centro de Salud Segovia Rural (Segovia)
Coordinador del Grupo de Trabajo de Neurología de la SEMERGEN
Comité Científico kNOW Alzheimer
18/08/2014

Cordell CB, Borson S, Boustani M, Chodosh J, Reuben D, Verghese J, Thies W, Fried LB; Medicare Detection of Cognitive Impairment Workgroup. Alzheimer’s Association recommendations for operationalizing the detection of cognitive impairment during the Medicare Annual Wellness Visit in a primary care setting. Alzheimers Dement. 2013; 9(2): 141-50.

Abstract

The Patient Protection and Affordable Care Act added a new Medicare benefit, the Annual Wellness Visit (AWV), effective January 1, 2011. The AWV requires an assessment to detect cognitive impairment. The Centers for Medicare and Medicaid Services (CMS) elected not to recommend a specific assessment tool because there is no single, universally accepted screen that satisfies all needs in the detection of cognitive impairment. To provide primary care physicians with guidance on cognitive assessment during the AWV, and when referral or further testing is needed, the Alzheimer’s Association convened a group of experts to develop recommendations. The resulting Alzheimer’s Association Medicare Annual Wellness Visit Algorithm for Assessment of Cognition includes review of patient Health Risk Assessment (HRA) information, patient observation, unstructured queries during the AWV, and use of structured cognitive assessment tools for both patients and informants. Widespread implementation of this algorithm could be the first step in reducing the prevalence of missed or delayed dementia diagnosis, thus allowing for better healthcare management and more favorable outcomes for affected patients and their families and caregivers.

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Artículo comentado

Dra. María Sagrario Manzano Palomo
Neuróloga. Hospital Infanta Cristina (Parla, Madrid)
Secretaria del Grupo de Demencias de la SEN
Comité Científico kNOW Alzheimer
16/06/2014

Rosenblum WI. Why Alzheimer trials fail: removing soluble oligomeric beta amyloid is essential, inconsistent, and difficult. Neurobiol Aging. 2013 Oct 19. [Epub ahead of print]

Abstract

Before amyloid formation, peptides cleaved from the amyloid precursor protein (APP) exist as soluble oligomers. These are extremely neurotoxic. Their concentration is strongly correlated with synaptic impairment in animals and parallel cognitive decline in animals and humans. Clinical trials have largely been aimed at removing insoluble beta amyloid in senile plaques and have not reduced soluble load. Even treatment that should remove soluble oligomers has not consistently reduced the load. Failure to significantly improve cognition has frequently been attributed to failure of the amyloid hypothesis or to irreversible alteration in the brain. Instead, trial failures may be because of failure to significantly reduce load of toxic Aβ oligomers. Moreover, targeting only synthesis of Aβ peptides, only the oligomers themselves, or only the final insoluble amyloid may fail to significantly reduce soluble load because of the interrelationship between these 3 points in the amyloid cascade. Thus, treatments may fail unless trials target simultaneously all 3 points in the equation-”triple therapy”. Cerebrospinal fluid analysis and other monitoring tools may in the future provide reliable measurement of soluble load. But currently, only analysis of autopsied brains can provide this data and thus enable proper evaluation and explanation of the outcome of clinical trials. These data are essential before attributing trial failures to the advanced nature of the disease or asserting that failures prove that the theory linking Alzheimer’s disease to products of amyloid precursor protein is incorrect.

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Artículo comentado

Dra. María Sagrario Manzano Palomo
Neuróloga. Hospital Infanta Cristina (Parla, Madrid)
Secretaria del Grupo de Demencias de la SEN
Comité Científico kNOW Alzheimer
14/04/2014

Cash DM, Ridgway GR, Liang Y et al.; Dominantly Inherited Alzheimer Network (DIAN). The pattern of atrophy in familial Alzheimer disease: Volumetric MRI results from the DIAN study. Neurology. 2013; 81(16): 1425-33.

Abstract

OBJECTIVE:To assess regional patterns of gray and white matter atrophy in familial Alzheimer disease (FAD) mutation carriers.

METHODS:A total of 192 participants with volumetric T1-weighted MRI, genotyping, and clinical diagnosis were available from the Dominantly Inherited Alzheimer Network. Of these, 69 were presymptomatic mutation carriers, 50 were symptomatic carriers (31 with Clinical Dementia Rating [CDR] = 0.5, 19 with CDR > 0.5), and 73 were noncarriers from the same families. Voxel-based morphometry was used to identify cross-sectional group differences in gray matter and white matter volume.

RESULTS: Significant differences in gray matter (p < 0.05, family-wise error-corrected) were observed between noncarriers and mildly symptomatic (CDR = 0.5) carriers in the thalamus and putamen, as well as in the temporal lobe, precuneus, and cingulate gyrus; the same pattern, but with more extensive changes, was seen in those with CDR > 0.5. Significant white matter differences between noncarriers and symptomatic carriers were observed in the cingulum and fornix; these form input and output connections to the medial temporal lobe, cingulate, and precuneus. No differences between noncarriers and presymptomatic carriers survived correction for multiple comparisons, but there was a trend for decreased gray matter in the thalamus for carriers closer to their estimated age at onset. There were no significant increases of gray or white matter in asymptomatic or symptomatic carriers compared to noncarriers.

CONCLUSIONS: Atrophy in FAD is observed early, both in areas commonly associated with sporadic Alzheimer disease and also in the putamen and thalamus, 2 regions associated with early amyloid deposition in FAD mutation carriers.

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Artículo comentado

Dr. Enrique Arriola Manchola
Geriatra. Responsable de la Unidad de Memoria y Alzheimer
Fundación Matia (San Sebastián)
Coordinador del Grupo de Demencias de la SEGG
Comité Científico kNOW Alzheimer
19/02/2014

Sura SD, RM Carnahan, Chen H, Aparasu RR. Prevalence and Determinants of Anticholinergic Medication Use in Elderly Dementia Patients. Drugs Aging 2013; 30: 837–44.

Abstract

BACKGROUND: People with dementia are sensitive to cognitive side effects of anticholinergic drugs. However, little is known about the prevalence of anticholinergic medications and its predictors in a nationally representative sample of community-based elderly dementia patients in the USA.

OBJECTIVES: The objectives of the study were to determine the prevalence and predictors of anticholinergic drugs use in elderly dementia patients.

METHODS: The study involved retrospective analysis of the 2005-2009 Medical Expenditure Panel Surveys (MEPS), a nationally representative sample of the non-institutionalized US population. The study evaluated annual prevalence of anticholinergic drug use during the study period and factors associated with the use of anticholinergics among community-dwelling persons aged 65 and older with dementia. The anticholinergic drugs were identified using the Anticholinergic Drug Scale (ADS). Multiple logistic regression within the conceptual framework of the Anderson Behavioral Model was performed to identify predictors associated with clinically significant anticholinergic drug (ADS level 2 or 3) use.

RESULTS: According to the MEPS, there were a total of 1.56 [95 % confidence interval (CI) 1.34, 1.73] million elderly dementia patients annually during the study period. Approximately, 23.3 % (95 % CI 19.2, 27.5) of elderly dementia patients used clinically significant anticholinergic agents (ADS level 2 or 3). Among the need factors, elderly dementia patients having mood disorders [odds ratio (OR) 2.19; 95 % CI 1.19, 4.06] and urinary incontinence (OR 6.58; 95 % CI 2.84, 15.29) were more likely to use drugs with clinically significant anticholinergic activities. Of the enabling factors, the odds of receiving higher-level anticholinergic drugs were significantly lower for patients who resided in the West region (OR 0.41; 95 % CI 0.17, 0.95) compared to the reference group, Northeast.

CONCLUSION: Over one in five elderly dementia patients used drugs with clinically significant anticholinergic effects. Mood disorder, urinary incontinence, and region were significantly associated with use of these drugs. Concerted efforts are needed to improve the quality of medication use by focusing on clinically significant anticholinergic agents.

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Artículo comentado

Dra. Rosa María Rodríguez Fernández
Neuróloga. Complexo Hospitalario Universitario de Ourense
Comité Científico kNOW Alzheimer
22/01/2014

Nordström P, Religa D, Wimo A, Winnblad B, Eriksdotter M. The use of cholinesterase inhibitors and the risk of myocardial infarction and death: a nationwide cohort study in subjects with Alzheimer’s disease. Eur Heart J. 2013; 34 (33): 2585-91.

Abstract

AIMS: Cholinesterase inhibitors (ChEIs) are used for symptomatic treatment of Alzheimer’s disease. These drugs have vagotonic and anti-inflammatory properties that could be of interest also with respect to cardiovascular disease. This study evaluated the use of ChEIs and the later risk of myocardial infarction and death.

METHODS AND RESULTS: The cohort consisted of 7073 subjects (mean age 79 years) from the Swedish Dementia Registry with the diagnoses of Alzheimer’s dementia or Alzheimer’s mixed dementia since 2007. Cholinesterase inhibitor use was linked to diagnosed myocardial infarctions (MIs) and death using national registers. During a mean follow-up period of 503 (range 0-2009) days, 831 subjects in the cohort suffered MI or died. After adjustment for confounders, subjects who used ChEIs had a 34% lower risk for this composite endpoint during the follow-up than those who did not [hazard ratio (HR) 0.66, 95% confidence interval (CI) 0.56-0.78]. Cholinesterase inhibitor use was also associated with a lower risk of death (HR: 0.64, 95% CI: 0.54-0.76) and MI (HR: 0.62, 95% CI: 0.40-0.95) when analysed separately. Subjects taking the highest recommended ChEI doses (donepezil 10 mg, rivastigmine >6 mg, galantamine 24 mg) had the lowest risk of MI (HR: 0.35, 95% CI: 0.19-0.64), or death (HR: 0.54, 95% CI: 0.43-0.67) compared with those who had never used ChEIs.

CONCLUSION: Cholinesterase inhibitor use was associated with a reduced risk of MI and death in a nationwide cohort of subjects diagnosed with Alzheimer’s dementia. These associations were stronger with increasing ChEI dose.

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