Cognitive dysfunction, mechanisms

Xiong H, Zeng YC, Zheng J, Thyhn M, Gendelman HE (1999) Soluble HlV-1 infected macrophage secretory products mediate blockade of long-term potentiation A mechanism for cognitive dysfunction in HIV-1-associated dementia [In Process Citation]. J Neurovirol 5 519-528. 

Ginkgo biloba54n positive response in depressed elderly patients with mild-to-moderate cognitive dysfunction and non-response history to therapeutic trials on tricyclic antidepressants additional research ongoing to clarify mechanism, efficacy in depression... 

So what does the next decade promise That we will treat smarter, with more specific treatments and vaccines that target cancer cells while leaving healthy cells intact. We will decipher even further how our brains react to diseases and therapies. And we will better understand the mechanisms behind cognitive dysfunction. 

Traditionally, most affective disorders have been treated with compounds that resemble the neurotransmitters that are deficient or in excess in specific brain regions. The aberrant levels of neurotransmitters (or their receptors), such as norepinephrine, dopamine, acetylcholine, and serotonin, have correlated with behavioral symptoms of schizophrenia, depression, anxiety, sleep disorders, motor dysfunctions, attention difficulties, and cognitive disorders. Most drugs discovered for these disorders resulted from screening compounds directly in rodent behavioral models that mimic the behavior of the disease. In these cases, the molecular target" or mechanism of action was assumed to be the deficiency or excess of a neurotransmitter. 

Taken together, the evidence for a specific deficit of hippocampal interneurons is accumulating. Together with the neuroimaging findings, this pattern points to a disinhibition of hippocampal pyramidal cells in schizophrenia. Future studies will explore the molecular mechanisms of hippocampal dysfunction in schizophrenia and it s impact on the cognitive and social function in schizophrenia. 

The availability of genetically modified mice has advanced our understanding of several neurodegenerative processes. Cellular neurobiology experiments have informed us about mechanisms of neuronal dysfunction in AD and PD mouse models. For instance, recent studies have identified that synaptic transmission is one of the earliest events in the cognitive abnormalities that characterize AD and PD. The integration of this information with data-based circuits modeling, in which neuronal electrical properties, synaptic transmission parameters, and brain oscillations can now be evaluated and it has been recently addressed in PD and AD. 

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