[Risk factors for Alzheimer's disease]. / Factores de riesgo de la enfermedad de Alzheimer.

AIM: In this review we present and discuss the main risk factors for Alzheimer's disease (AD) reported by epidemiological, genetic and biochemical studies. DEVELOPMENT: The most frequently mentioned factors are: 1. Age. It is the principal marker for the disease risk; 2. Sex. It is estimated that the prevalence of AD is higher in women than in men; 3. Genetics. Although the genetic role has been demonstrated, there is an important genetic heterogeneity; 4. Tobacco. Various studies have found a protective effect, however this effect could be attributed to survival bias; 5. Alcohol. The regular consumption of alcohol was associated with reduced incidence of AD, especially with wine consumption; 6. Family history of dementia. Nearly 40% of persons with AD have family history of dementia; 7. Non steroidal antiinflammatories (NSAIDs). The use of NSAIDS could help in reducing the symptoms of the disease or even avoid them; 8. Craneoencephalic trauma. The role of the craneoencephalic trauma is controversial; 9. Education. The increase of AD in low education persons was published; 10. Diet. The consumption of antioxidants in diet o in supplementary forms appears to be neuroprotector. CONCLUSIONS: The grand variety of published epidemiological studies with different methodology makes it difficult to find homogeneous results. This leaves us controversial impressions about how to prevent the disease.

[Meta-analysis: the science of review in Neurology]. / Metaanálisis: la ciencia de la revisión en Neurología.

INTRODUCTION: The review and continuous analysis of the present knowledge have always been necessary for scientific and clinical practice advance. This study presents the difference between narrative and systematic reviews, the most important points of meta-analysis, and finishes with detailed description of its phases. Our objective was to explain, in simple terms, the technique of meta-analysis and this could permit its application and use in the clinical practice and neurological investigations. DEVELOPMENT: The term meta-analysis was described for the first time by the psychologist Glass in 1967. Since then, the meta-analysis was utilized by many investigators as a technique to combine the results of different studies. The steps of a meta-analysis are: 1. Hypothesis of the study; 2. Localization of the studies of investigation; 3. Selection of the localized studies; 4. Qualitative meta-analysis; 5. Quantitative meta-analysis. Basically, It refers to the numeric combination of data, which were extracted by the reviewers. The mathematical method which will be used to evaluate the effect size should be chosen, also homogeneity and sensibility tests should be done. CONCLUSIONS: Well-designed meta-analysis is accepted as the optimum form to present the results of different studies. The meta-analysis could be of great importance for clinical practice and neurological research.

[Young onset Parkinson's disease and smoking: meta-analysis]. / Enfermedad de Parkinson temprana y tabaco: metanálisis.

INTRODUCTION: Previous systemic reviews have reported a protective effect of smoking against Parkinson's disease (PD). However, the protective effect has not been examined before by any systemic review in patients with young onset PD. OBJECTIVE: Examine the association between young onset PD and tobacco smoking. MATERIAL AND METHODS: We conducted a meta-analysis including all published observational studies that investigated this association before January 2003. All languages were included with no restriction for year of publication. Risk estimate and its 95% confidence interval (95% CI) were extracted or calculated for all localized studies in patients with young onset PD. RESULTS: Five case-control studies investigated the association between young onset PD risk and ever smoking. The fixed-effect pooled analysis was 0.55 (95% CI: 0.38 0.81), with insignificant homogeneity test. CONCLUSIONS: This meta-analysis shows a protective effect of tobacco smoking against young onset PD. Our results coincide with the other reviews which did not consider the age of diagnosis of PD. However, it is highly recommended prospective studies for the association between young onset PD risk and ever smoking

[Parkinson s disease risk factors]. / Factores de riesgo en la enfermedad de Parkinson.

AIMS: In this review we present and discuss the main risk factors (RF) for Parkinson s disease (PD) reported by epidemiological and biochemical research. METHODS: The most frequently mentioned RF are: 1. Age: PD is not a pathological condition that is restricted to the elderly, although most people who suffer from it are over 60 years of age; 2. Sex: in most epidemiological studies there are no differences to be found in prevalence of PD according to sex; 3. Genetic: no gene has been identified as being responsible for idiopathic PD. Nevertheless, family antecedents of PD have been identified as RF; 4. Craneoencephalic trauma: this factor can have a systematic bias, since patients seek an explanation for their illness and remember any head injury as its possible cause; 5. Neurotoxins: a great deal of research was focused on the relation between PD and direct or indirect exposition to compounds such as MPTP, used in pesticides; 6. Antioxidants: it is thought that if ingested in sufficiently high quantities, either as part of the diet or in the form of supplements, they might reduce the risk of PD or slow down its progress; 7. Smoking: several studies have shown a negative relation, while other studies found no significant relation. CONCLUSIONS: There are several RF for PD, although no single decisive triggering factor has been found to date. Future research must consider the hypothesis of a multifactor aetiology and take into account the interaction between genetic and environmental factors.

[Parkinson's disease, tobacco and age: meta analysis]. / Enfermedad de Parkinson, tabaco y edad: metanálisis.

INTRODUCTION: Epidemiological studies have demonstrated contradictory results about the association between smoking and the risk of Parkinson s disease (PD). OBJECTIVE: Examine the hypothesis of the EUROPARKINSON group that smoking protects against PD only in patients below 75 years of age. MATERIAL AND METHODS: We conducted a meta analysis including all observational studies that were published about this association before January 2001. All languages were included with no restriction for year of publication. Risk estimate and its 95% confidence interval (95% CI) were extracted or calculated for all localized studies in patients below or above 75 years of age. RESULTS: Seventeen studies investigated the association between PD risk and smoking in patients below 75 years of age. Meanwhile, only seven studies investigated the association in patients above 75 years of age. The fixed effect pooled analysis in patients below 75 years of age was 0.59 (95% CI: 0.52 0.67), with insignificant homogeneity test. Patients above 75 years of age had fixed effect pooled analysis of 0.76 (95% CI: 0.59 0.99), with insignificant homogeneity test. CONCLUSIONS: The pooled analysis in patients below 75 years of age clearly demonstrates that smoking is inversely associated with PD risk. The 95% CI of the pooled analysis in patients above 75 years of age is nearly overlapping unity. This result is not in favor for the negative association in old patients, and confirms the hypothesis of the EUROPARKINSON group.

Parkinson's disease, smoking and family history: meta-analysis.

To estimate the pooled risk of tobacco smoking for Parkinson's disease (PD) in patients with and without PD family history. We conducted systematic searches of Medline, PsycLIT, Embase, Current contents, Best Evidence, Nisc Mexico Biblioline, previous reviews, examination of cited reference sources and personal contact and discussion with several investigators expert in the field. Studies in all languages were considered. Published observational studies on PD and cigarette smoking stratified by PD family history were reviewed. When two or more papers were based on an identical study, the paper that principally investigated the relationship between PD, smoking stratified by PD family history or the paper that was published last was used. Three case-control studies were carried out between 1996 and 2000, of which one reported risk estimates. The risk of ever smoker in patients with positive PD family history was 0.82 (95% confidence interval 0.44-1.53). There was an obvious protective effect in the pooled estimate in patients with negative PD family history [odds ratio 0.77 (95% confidence interval 0.59-1.01)]. Although our pooled estimates show that smoking is inversely associated with the risk of PD only in patients with negative PD family history, further studies evaluating the interaction between smoking and PD family history are strongly needed.

[Parkinson's disease and smoking: coherence and plausibility]. / La enfermedad de Parkinson y el tabaco: coherencia y plausibilidad.

INTRODUCTION: Many studies have shown that smoking is lower in patients with Parkinson s disease. However, in other investigations this was not observed. The various studies involved showed wide variation with regard to methodology, criteria for diagnosis and periods of observation and hence it is difficult to compare them. DEVELOPMENT: The first studies published were designed to examine the effects of smoking in general and information was obtained regarding the possible disorders related to tobacco smoking according to the records of mortality, which may contain errors due to selective mortality and mistaken diagnosis. Most of the studies of cases and controls included prevalent cases which accepted the study, mainly hospital cases. Also it is probable that the prevalent cases of Parkinson s disease do not smoke because of their disorders of movement. CONCLUSIONS: Many researchers have found important information about the pathophysiology of Parkinson s disease and its association with smoking. However, the hypothesis regarding the association between smoking and low risk of Parkinson s disease are various and independent, apart from the hypothesis of a truly biological mechanisms. Since the subject is still controversial, systematic reviews together with epidemiological and experimental studies are necessary.