Therapeutic Approaches for AD

Cell therapy is a potential therapeutic approach for AD. Tricyclodecan-9-yTxanthogenate (D609) was used to induce human mesenchymal stem cells isolated from Wharton jelly of the umbilical cord (HUMSCs) to differentiate into neuron-like cells... 

Microglial-mediated neuroinflammation and neurotoxicity are involved in the pathogenesis of AD. Regulation of microglial activation and suppression of neurotoxic proinflammatory molecules may provide a potential therapeutic approach for the treatment of... 

Currently the only specific pharmacological therapeutic option available for AD patients is treatment with cholinesterase inhibitors, which provide moderate benefits in a subset of patients for a limited period [7]. More efficient future therapeutic strategies may be directed at the metabolic events resulting in Ap accumulation, for example by inhibition of P- or y-sec-retase [7], or at the prevention of neuronal loss by neurotrophin therapy [6]. The availability of transgenic mouse models of the disease, such as mice overexpressing APP mutants [8], and the utilization of primate models of cerebral amyloid [9] permits preclinical testing of novel diagnostic and therapeutic approaches. 

Perhaps psychopharmacological treatments for psychotic disorders in the future will need to borrow a chapter out of the book of cancer chemotherapy and HIV/ AIDS therapy, in which the standard of treatment is to use multiple drugs simultaneously to attain therapeutic synergy. Combination chemotherapy for malignancy uses the approach of adding together several independent therapeutic mechanisms. When successful, this results in a total therapeutic response that is greater than the sum of its parts. 

Doerfler A, Forsting M, Reith W, Staff C, Heiland S, Schabitz WR, von Kummer R, Hacke W, Sartor K (1996) Decompressive craniectomy in a rat model of malignant cerebral hemispheric stroke experimental support for an aggressive therapeutic approach. J Neurosurg 85 853-859 Elster AD (1991) MR contrast enhancement in brainstem and deep cerebral infarction. Am JNeuroradiol 12 1127-1132 Endres M, Dirnagl U (2002) Ischemia and stroke. Adv Exp Med Biol 513 455-473... 

The proteomic analysis of the brain has certain limitations that are related either to the sample and/or analytical approach. In the analysis of the brain, many factors may be involved, such as differences among individuals, differences in age and sex, possible other diseases, treatment with medicines, as well as technical factors, disease-unrelated factors, such as postmortem time, improper treatment of the samples, etc., all of which can affect a clear discrimination between healthy and diseased states of interest. The technical limitations involve inefficient detection of low-abundance gene products, hydrophobic proteins (they do not enter the IPG strips), and acidic, basic, high-, and low-molecular mass proteins. All these protein classes are underrepresented in 2-D gels (Lubec et al., 2003 Fountoulakis, 2004). A combination of proteomics methods with protein separation, enriching techniques, and alternative methodologies for detection will improve the detection of additional differences between AD and control brains. Such differences may be essential in the discovery of early disease markers and therapeutic approaches. 

Therapy is generally the same for acquired immune deficiency syndrome/non-acquired immune defidency syndrome patients except where indicated and should be continued for 2 weeks after the last positive blood culture and resolution of signs and symptoms of infedion. All patients should receive an ophthalmologic examination. Amphotericin B may be switched to fluconazole (intravenous or oral) for the completion of therapy. Susceptibility testing of the infecting isolate is a useful ad und to species identification during seledion of a therapeutic approach because it can be used to identity isolates that are unlikely to respond to fluconazole or amphotericin B. However, this is not currently available at most institutions. 

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