Search

Background: Cancer and degenerative diseases share some pathogenic mechanisms which act in opposition to one another to produce either uncontrolled cell proliferation or cell death. According to several studies, patients with Alzheimer disease have a lower risk of neoplasia, and vice versa. This study describes the prevalence of tumours (active or successfully treated) in a series of patients with and without a dementing degenerative disease treated at a cognitive neurology unit., Patients and Method: We analysed the frequency and topography of tumours and the presence or absence of a neurodegenerative disease in a group of 1,164 patients. Neurodegenerative diseases were classified in 4 groups: Alzheimer disease, synucleinopathies, Pick complex, and polyglutamine complex. We subsequently compared tumour frequency in patients with and without a degenerative disease, and prevalence of neurodegenerative diseases in patients with and without tumours., Results: Tumours were detected in 12.1% of the patients with a neurodegenerative disease and in 17.3% of the remaining patients. Around 14.8% of the patients with a history of neoplasia and 20.8% of the patients with no history of neoplasia were diagnosed with a neurodegenerative disease. Except for these differences and the differences between subgroups (type of degenerative disease and tumour location) were not statistically significant, except when comparing neurodegenerative diseases to central nervous system tumours, and synucleinopathies to neoplasms., Conclusion: Dementing degenerative diseases and neoplastic disorders are not mutually exclusive. Nevertheless, the rate of co-occurrence is lower than would be expected given the prevalence rate for each group., (Copyright © 2017 The Authors. Publicado por Elsevier España, S.L.U. All rights reserved.)

Introduction: Presently article carried out an up-to-date revision of the literature on the diagnosis of the Parkinson's disease, considering the clinical aspects, those of neuroradiology and the genetic diagnosis., Development: The Parkinson's disease is the second most common neurodegenerative disorder and despite of the important development that has taken place in the last years as much in molecular genetics and neuroradiology, the diagnosis of this disease continuous being eminently clinical, the appropriate knowledge of the calls 'cardinal signs' and its application in the diagnosis increases the possibility that this it is guessed right, regrettably the definitive approach is only obtained in the autopsy. The genetic studies and of neuroradiology mainly are presented as tools for a more reliable differential diagnosis with other parkinsonism forms and the knowledge of these techniques can be useful in the taking of therapeutic decisions or of the affected patient's integral treatment. They have also been different monogenic forms in origin to the sporadic form of the illness., Conclusion: The knowledge and search of the preponderant clinical signs increases the capacity of diagnostic of the illness, in the same way the appropriate use of additional methods of investigation, mainly in the differential diagnosis.

Introduction and Method: The uncertainty regarding the nosology and significance of Lewy bodies (LB) in dementia is still very present in current research. It is an acknowledged fact that an important number of cases of Alzheimer s disease (AD) also present LB. These can be detected by a synuclein immunohistochemistry in most of the sporadic cases of AD and is most frequently detected in the amygdala., Conclusions: Although the role of LB and the filaments of Lewy in the pathogenesis of dementia has still to be determined, it is clear that alphya-synuclein immunohistochemistry represents an important advance in the evaluation of the neuropathological changes in AD and in associated dementias.

The term alpha-synucleinopathy is used to name a group of disorders having in common the abnormal deposition of alpha-synuclein in the cytoplasm of neurons or glial cells, as well as in extracellular deposits of amyloid. In Parkinson's disease and Lewy body dementia, alpha-synuclein is the main component of Lewy bodies and dystrophic neurites; alpha-synuclein also accumulates in the cytoplasm of glial cells. In multiple system atrophy, alpha-synuclein conforms the cytoplasmic oligodendroglial inclusions and the neuronal inclusions which are the hallmark of this disease. Finally, the amyloidogenic fragment 61-95 amino acids of alpha-synuclein is the non-Abeta component of senile plaque amyloid in Alzheimer disease. Accumulations of alpha-synuclein in all these disorders have in common a fibrilar configuration, but they differ in the binding of alpha-synuclein to distinct proteins with the exception of ubiquitin whose binding to alpha-synuclein is common to all alpha-synuclein inclusions. The mechanisms leading to alpha-synuclein fragmentation and aggegation into extracellular amyloid are not known, although alpha-synuclein fragment and betaA4 aggregates are the result of abnormal cleavage of large precursors. On the other hand, several studies have shown that alpha-synuclein may adopt a fibrilar conformation and give rise to insoluble forms and high molecular weight aggregates in vitro. Similar complexes have also been observed in alpha-synucleinopathies. Although studies in vitro and in vivo have shown toxic effects of alpha-synuclein, the consequence of alpha-synuclein deposition on cell survival in alpha-synucleinopathies is not known.