Introduction. Currently used antiparkinsonian drugs neither stop nor slow-down the progressive nature of the disease. The final phase of PD is characterized by the presence of symptoms and signs resistant to dopaminergic agents, such as depression, dementia, freezing and falls. Therefore, it is urgent to developtherapies able to positively modify this outcome. Despite neuroprotection is a research priority in PD, no effective strategies have been found so far.Method. A key informants study was conducted. A group of experts in PD fulfilled a questionnaire of 10 questions to explore the most important topics related to neuroprotection. Afterwards a consensus about the cur-rent situation of neuroprotection in PD was established and future directions of development were suggested.Results. Most of the answers emphasized the need of new concepts, the limitations of animal models and the difficulties in the difficulties in demonstrating a neuroprotective effects in humans owing to a lack of biomarkers. Some of the experts believe that we are already exerting a disease modifying effect.Conclusions. The concept of neuroprotection should be widened. Animal models should be improved. A reliable biomarker to start neuroprotective therapies long before the appearance of motor symptoms and to evaluate the neuroprotective effect of any therapy should be urgently developed.

Introduction. Currently used antiparkinsonian drugs neither stop nor slow-down the progressive nature of the disease. The final phase of PD is characterized by the presence of symptoms and signs resistant to dopaminergic agents, such as depression, dementia, freezing and falls. Therefore, it is urgent to develop therapies able to positively modify this outcome. Despite neuro-protection is a research priority in PD, no effective strategies have been found so far. Method. A key informants study was conducted. A group of experts in PD fulfilled a questionnaire of 10 questions to explore the most important topics related to neuroprotection. Afterwards a consensus about the cur-rent situation of neuroprotection in PD was established and future directions of development were suggested. Results. Most of the answers emphasized the need of new concepts, the limitations of animal models and the difficulties in the difficulties in demonstrating a neuroprotective effects in humans owing to a lack of biomarkers. Some of the experts believe that we are already exerting a disease modifying effect. Conclusions. The concept of neuroprotection should be widened. Animal models should be improved. A reliable biomarker to start neuroprotective therapies long before the appearance of motor symptoms and to evaluate the neuroprotective effect of any therapy should be urgently developed.

Independent deletion of the PARK2 gene and hTauVLW over-expression in mice produce mild alterations in the brain. However, the presence of both mutations in a parkin-deficient and hTauVLW double mutant mouse causes a tau neuropathology, reactive astrocytosis, and neuronal loss in the cortex and hippocampus, as well as lesions in nigrostriatal and motor neurons. Moreover, these mutants display some memory and exploratory defects that reflect a functional link between parkin and tau proteins. We have tested the motor activity and coordination of these double mutant mice to determine the effects of parkin deletion in mice over-expressing the hTauVLW transgene. While the loss of parkin alone produces increased exploration and alterations in gait and motor coordination, in hTauVLW transgenic mice the absence of parkin causes less prominent motor impairments. These effects suggest the existence of some compensatory mechanisms that are activated when the hTauVLW transgene is over-expressed in the absence of parkin. This mouse model will hopefully help to study the causes of the motor deficits associated with certain neuropathologies related to the tau and parkin proteins, and to find appropriate treatments.

Uno de los campos de la medicina que mas expectativas ha levantado en los ultimos anos es la terapia celular con celulas madre. El aislamiento de celulas embrionarias humanas, la aparente e inesperada potencialidad de las celulas madre adultas y el desarrollo de la terapia genica nos llevar a imaginar un futuro esperanzador para un importante numero de enfermedades actualmente incurables. A lo largo de las siguientes paginas vamos a tratar de dibujar el panorama de la investigacion con celulas madre, describiendo los principales logros en este campo asi como algunas de las preguntas pendientes de responder. A pesar de las grandes expectativas, es fundamental que mantengamos un espiritu critico y realista a la hora de analizar los avances cientificos en esta area.

Introduction. Parkinson's disease (PD) is a quite heterogeneous disorder thus difficulting the interpretation of transversal studies. Patients' registries and longitudinal studies can be considered as a priority in order to understand many still unknown aspects of the disease. Aim. To create and follow in a longitudinal way a cohort of 300 patients with de novo PD who will be assessed and treated in a uniform way. The end-point of the project will be the donation of the brain. Development. This is a non-hypothesis driven project which immediate steps are: a) Inclusion of de novo PD patients; b) Application of a protocol of evaluations and treatment recommendations; c) Obtaining and maintenance of biological samples; d) Elaboration of a data base to be released on-the net; e) Design and start of different studies to be performed simultaneously; and f) Brain donation. The study will be carried out by the Consorcio Parkinson across the country. Retrospective and prospective studies to be addressed in the future are of quite diverse nature, from clinical to molecular.

Introduction and development. Parkinson's disease (PD) is a chronic and progressive disorder It produces a significant burden not only for patients, but also for their family and caregivers, with a major socio-economic impact on society. Current knowledge on PD is characterized by scarce information about the evolutionary course of: 1) the non-motor PD features; 2) impact of non-motor PD features on disability and health related quality of life (HRQL) impairment; 3) factors related to disability and HRQL determinants; 4) factors that speed or slow the progression of PD; 5) differential long-term effect of available PD therapeutic schedules and their relationships with disability, complications, and HRQL; and 6) impact of the disease on patients' caregivers. In addition, heterogeneity in the metric quality of the applied measures and selection bias are frequently found Conclusion. Due to the aforementioned limitations and from a multidimensional perspective, a new longitudinal study in PD is deemed necessary. The longitudinal study of PD patients (ELEP) includes a long-term follow-up of never before sistematically assessed aspects, will allow to increase the global knowledge about PD.

One of the fields of medicine that has raised the most expectations in recent years is cell therapy with stem cells. The isolation of human embryo cells, the apparent and unexpected potentiality of adult stem cells and the development of gene therapy lead us to imagine a hopeful future for a significant number of diseases that are at present incurable. In this article we will sketch out the panorama of stem cell research, describing the main achievements in this field as well as some of the questions that await an answer. In spite of the great expectations, it is essential that we maintain a critical and realistic spirit when it comes to analysing the scientific advances in this area.

The most widely accepted criteria for Alzheimer's disease (AD) diagnosis (NINCDS-ADRDA and DSM-IV) do not allow to differentiate accurately between AD and other degenerative dementias which have recently formulated criteria for its clinical diagnosis. Therefore, it is necessary to bring AD diagnostic criteria up to date in order to optimise their specificity, by assessing its most specific clinical manifestations, its most representative markers and those features typical of other diseases which are usually taken into account for a differential diagnosis. According to the latest reports on the subject, the disturbances suffered by memory, behaviour and the rest of cognitive and executive functions must be equally considered when establishing the syndromic diagnosis of dementia; this will always require the coexistence of an evident functional impairment. Due to this, the concepts of and cognitive should be clearly distinguished. For the time being, AD can only be diagnosed when dementia has been proved and this shows a series of cognitive, behavioural and neurological features which are representative of it. Nevertheless, some diagnostic markers appear to be precocious and specific enough to try to identify those patients who suffer from mild cognitive impairment due to an incipient stage of AD. We are suggesting some criteria for the clinical diagnosis of dementia, mild cognitive impairment and AD that seem to be more detailed and probably more specific than the existing ones.