Alzheimer Disease: From Molecular Biology to Theraphy by Luigi Amaducci, Marzia Baldereschi (auth.), Robert E.
By Luigi Amaducci, Marzia Baldereschi (auth.), Robert E. Becker, Ezio Giacobini, Joyce M. Barton, Mona Brown (eds.)
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Additional resources for Alzheimer Disease: From Molecular Biology to Theraphy
REFERENCES Blessed G (1990): Definition and classification of the dementias: the point of view of a clinician. In: Innovative Trends in Psychogeriatrics. Interdiscipl Top in Gerontol. Wertheimer J, Bauman P, Gaillard M, Schwed Peds. Basel: Karger pp 63-9. Bouras C, Hof P (1992): Neuropathologie de la maladie d'Alzheimer In: Editions techniques. Enc Med Chir Psychiatr 37280 A20. Bucht G, Adolfsson R, Lithner et al. (1983): Changes in blood glucose and insulin secretion in patients with senile dementia of Alzheimer type.
Alzheimer neurofibrillary degeneration can probably be inhibited by increasing the tau-phosphatase activity in the brain of patients with AD. ACKNOWLEDGMENTS Secretarial support was provided by Joanne Lopez and Maritza Kaufmann. This work was supported in part by funds from the New York State Office of Mental Retardation and Developmental Disabilities, National Institutes of Health Grants AG05892, AG08076, NS18105, TW00507, and Zenith Award from the Alzheimer's Association, USA. REFERENCES Alonso A del C, Zaidi T, Grundke-Iqbal I and Iqbal K (1994): Role of abnormally phosphorylated tau in the breakdown of microtubules in Alzheimer disease.
Thus, the abnormal hyperphosphorylation of tau appears to lead to the sequestration of normal tau by the aberrant tau, causing inhibition of assembly and disruption of preformed microtubules, and the accumulation of the tau as tangles of Alzheimer Neurofibrillary Degeneration 33 filaments. The latter subsequently, by as yet not fully understood mechanisms, are converted into PHF tangles. The disruption of the microtubule system in the affected neurons probably leads to compromised axonal transport and eventually a retrograde degeneration of the affected neurons.