A New Focus on Cytoskeletal Therapy in Alzheimer’s Disease
The classical approach to Alzheimer’s Disease (AD) starts from the neuropathological findings and assumes any reasonable model should at least incorporate either β-amyloid plaques or neurofibrillary tangles. However, these neuropathological features are just tombstones of a disease process going on for several years. In the absence of specific and sensitive imaging markers for these aberrant protein forms, we will not be able to judge properly on their relevance to the course of the pathology per se.
KeywordsSerotonin Neurol Tryptophan Neuroblastoma Butyrate
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- Moechars D, Lorent K, De Strooper B, Dewachter I, van Leuven F (1996): Expression in brain of APP mutated in the α-secretase site, causes disturbed behavior, neuronal degeneration and premature death in transgenic mice. EMBOJ, in press.Google Scholar
- Nikolic M, Delalle I, Tsai L (1995): The role of p35/cdk5 kinase in neuronal differentiation and neurite outgrowth. Soc Neurosci Abst, 21. part 3, p2001Google Scholar
- Nuydens R., De Jong M., Nuyens R., Cornelissen F, Geerts H (1996): Aberrant tau phosphorylation decreases fast axonal transport. (Submitted).Google Scholar
- Richard S, Brion JP, Couck AM, Flament-Durand J (1985): Accumulation of smooth endoplasmic reticulum in Alzheimer’s disease: new morphological evidence of axoplasmic flow disturbances. J. Submicr. Cytol Pathol 21:461–465.Google Scholar
- Scott S, Mufson E, Weingartner J, Skau K, Crutcher K (1995): Nerve Growth factor in Alzheimer’s disease: increased levels throughout the brain coupled with declines in Nucleus basalis. Journ Neurosci 15:6213–6221.Google Scholar
- Zheng Y, Jiang M, Trumbauer M, Sirinathsinghji D, Hopkins R, Smith D, Heavens R, Dawson G, Boyce S, Connor M, Stevens K, Slunt H, Sisodia S, Chen H, Van der Ploeg L (1995): β-amyloid precursor protein deficient mice show reactive gliosis and decreased locomotor activity. Cell 81:525–531.PubMedCrossRefGoogle Scholar