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We describe the history of the histochemical stains that contributed most to the development of modern pathology during the last two centuries. Histochemical stains are presented in a list, which provides the essential information about year, country and main use of each to enable the reader to follow the chronological and geographical history of histochemistry. In addition to the historical evaluation of histochemistry development, we investigate how many classical histochemical stains survive in a modern laboratory of pathology and how often they are used for diagnostic practice compared to immunohistochemical (IHC) techniques. A ratio of about one histochemical reaction to 13 IHC reactions was tabulated. Finally, our data make it possible to define different cultural approaches to the terminology of histochemical and IHC stains: the former were based on eponyms, which link the stain with the name of its inventor, while the latter use a more impersonal biological terminology. [ABSTRACT FROM AUTHOR]

Historically, pharmacotherapy for schizophrenia was mainly focused on finding drugs to treat psychotic symptoms only, without addressing other crucial domains of the disorder such as cognitive impairments. As a result, these domains have remained undertreated. In this review, we discuss recent preclinical research efforts, including investigation of synaptic mechanisms as well as intracellular signalling pathways and mechanisms involved in neuroplasticity and cell resilience, that may represent new mechanisms participating in the pathogenesis of schizophrenia, particularly at the level of the prefrontal cortex and hippocampus, and that might lead to the development of drugs that can counteract, at least partially, the cognitive impairments typical of schizophrenia. [ABSTRACT FROM AUTHOR]

Finding an effective therapy to treat chronic neurodegenerative disorders still represents an unmet and elusive goal, mainly because so many pathogenic variables come into play in these diseases. Recent emphasis has been placed on the role of neurotrophic factors in the aetiology of such disorders because of their role in the survival of different cell phenotypes under various adverse conditions, including neurodegeneration.This review summarizes the current status and the efforts to treat neurodegenerative disorders by the exogenous administration of neurotrophic factors in an attempt to replenish trophic supply, the paucity of which may contribute to the development of the illness. Although promising results have been seen in animal models, this approach still meets disparate and often insurmountable problems in clinical settings, presumably related to the unique nature of the human being. [ABSTRACT FROM AUTHOR]

Background: Brain-Derived Neurotrophic Factor (BDNF) is a neurotrophin which plays survival- and growth-promoting activity in neuronal cells and it is involved in cellular plasticity mechanisms as it controls activity dependent synaptic transmission. A functional polymorphism (Val66Met) in the pro-region of BDNF, which affects the intracellular trafficking of proBDNF has been associated with memory and cognitive deficits as well as to an increased susceptibility for several psychiatric disorders especially those with a neurodevelopmental origin. To date, no study has evaluated the influence of the Val66Met polymorphism on BDNF levels in a peripheral system that may reflect fetal neurodevelopment. Therefore we investigated in amniotic fluids (AF) obtained from 139 healthy women during 15-17 week of pregnancy, BDNF protein levels in correlation with the Val66Met polymorphism.Results: Interestingly we found a significant BDNF protein levels reduction in 55 Met carriers (Val/Met and Met/Met) (p = 0.002) as compared to 84 non carriers (Val/Val), and no effect of fetus gender, maternal age or gestation week on BDNF levels has been observed.Conclusion: These results, although explorative, indicate that during fetal life the Val66Met genotype might influences BDNF protein levels in AF supporting the involvement of this polymorphism in behavioral and functional brain individual differences in the adulthood. [ABSTRACT FROM AUTHOR]