Glucocorticoid Effects On Central Nervous Excitability And Synaptic Transmission
Neurosciences & Neurology
Hall E D
International Review of Neurobiology
1982
1905-06
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1016/s0074-7742(08)60625-x" target="_blank" rel="noreferrer noopener">10.1016/s0074-7742(08)60625-x</a>
Synaptic plasticity and secondary epileptogenesis.
Animals; Epilepsy/etiology/*physiopathology; Humans; Long-Term Potentiation/physiology; Neuronal Plasticity/*physiology; Synapses/*physiology
Teyler T J; Morgan S L; Russell R N; Woodside B L
International review of neurobiology
2001
1905-06
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/s0074-7742(01)45014-8" target="_blank" rel="noreferrer noopener">10.1016/s0074-7742(01)45014-8</a>
Multimodal drugs and their future for Alzheimer's and Parkinson's disease.
Alzheimer Disease/*drug therapy/*enzymology/prevention & control; Animals; Combined Modality Therapy/*methods; Forecasting; Humans; Monoamine Oxidase Inhibitors/*pharmacology/therapeutic use; Parkinson Disease/*drug therapy/*enzymology/prevention & control
This chapter discusses the rationale for developing multimodal or multifunctional drugs (also called designed multiple ligands or DMLs) aimed at disease-modifying treatment strategies for the most common neurodegenerative diseases Alzheimer's and Parkinson's disease (AD and PD). Both the prevalence and incidence of AD and PD have seen consistent and dramatic increases, a disconcerting phenomenon which, ironically, has been attributed to extended life expectancy brought about by better health care globally. In spite of these statistics, the development and introduction to the clinic of new therapies proven to prevent or delay the onset of AD and PD have been disappointing. Evidence has accumulated to suggest that the etiopathology of these diseases is extremely complex, with an array of potential drug targets located within a number of deleterious biochemical pathways. Therefore, in these diseases, it is unlikely that the complex pathoetiological cascade leading to disease initiation or progression will be mitigated by any one drug acting on a single pathway or target. The pursuit of novel DMLs may offer far better outcomes. Although certainly not the only, and perhaps not even the best, approach but farthest along the drug development pipeline in the DML paradigm are drugs that combine inhibition of monoamine oxidase with associated etiological targets unique to either AD or PD. These compounds will constitute the major focus of this chapter, which will also explore radically new paradigms that seek to combine cognitive enhancers with proneurogenesis compounds.
Van der Schyf Cornelis J; Geldenhuys Werner J
International review of neurobiology
2011
1905-07
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/B978-0-12-386467-3.00006-6" target="_blank" rel="noreferrer noopener">10.1016/B978-0-12-386467-3.00006-6</a>