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D. Auld, T. Kornecook, S. Bastianetto, R. Quirion (2002)
Alzheimer’s disease and the basal forebrain cholinergic system: relations to β-amyloid peptides, cognition, and treatment strategiesProgress in Neurobiology, 68
M. Tuszynski, H. U, J. Alksne, R. Bakay, M. Pay, D. Merrill, L. Thal (2002)
Growth factor gene therapy for Alzheimer disease.Neurosurgical focus, 13 5
Tuszynski MH, Thal L, Pay M et al. A phase 1 clinical trial of nerve growth factor gene therapy for Alzheimer disease. Nat Med 2005: 6: 551–5. Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is the most common form of senile dementia. It is characterized by gradual memory loss that begins during the early stages of the disease. As the disease progresses, deterioration of higher cortical function (confusion and disorientation) and behavioral disturbances (depression, agitation, and delusion) occur, eventually leaving affected individuals unable to care for themselves. The primary neuropathological hallmarks of AD consist of extracellular plaques of aggregated ॆ-amyloid protein, intracellular neurofibrillary tangles containing hyper-phosphorylated tau protein, and progressive loss of cortical and subcortical neurons. Selective degeneration of the cholinergic neurons of the nucleus basalis is one of the earliest pathological events in AD ( 1 ). To date, only symptomatic therapeutic agents have been approved for the treatment of AD, such as the acetyl-cholinesterase inhibitors and the non-competitive N-Methyl-d-Aspartate (NMDA)-receptor antagonist memantine. Disease-altering treatments that prevent neuronal loss and/or enhance neuronal function are desperately needed. Ex vivo gene therapy is one such novel therapeutic approach in which autologous cells are genetically modified in vitro
Clinical Genetics – Wiley
Published: Sep 1, 2005
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