By C. L. Masters, K. Beyreuther (auth.), C. L. Masters M.D., K. Beyreuther Ph.D., M. Trillet Prof., Y. Christen Ph.D. (eds.)
This publication summarizes the final ten years' examine on Alzheimer's affliction. Genetic mutations within the gene which codes for amyloid precursor protein (APP) have now been proven to reason Alzheimer's disorder in a few households. different genetic loci are actually being chanced on which relate to Alzheimer's affliction in a few households. realizing the conventional constitution and serve as of the APP gene product will ultimately supply avenues for constructing particular healing recommendations precise on the amyloid deposition within the Alzheimer's disorder mind. medicinal drugs which may inhibit or dissolve the amyloid, impact the synthesis and proteolysis of APP, or which keep an eye on the job of the APP gene all carry the promise of finally yielding an efficient therapy for Alzheimer's ailment.
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Additional resources for Amyloid Protein Precursor in Development, Aging and Alzheimer’s Disease
This finding is similar to mammalian APP transcripts that are abundant in fetal tissues and in adult stages (Kitaguchi et al. 1988; Tanzi et al. 1988). These observations have been substantiated by immunolocalization of the APPL protein using C(-APPL serum. APPL protein is observed in neuronal cell bodies and in neuronal processes (Luo et al. 1990). Figure 2 shows APPL immunoreactivity in the photoreceptors in developing eye primordia; the developing eye primordia is connected to the optic lobes in the central nervous system by the optic nerve.
Moreover, mutants of the APP gene have been isolated from patients suffering from familial Alzheimer's disease. Several amino acid substitutions have been identified in different families. Common to them all is their location close to or even within the f3A4 region (Hardy 1992 (review); Citron et al. 1992; Carter et al. 1992). Together these results strongly support the hypothesis that Alzheimer's disease is due to a metabolic defect of APP which results in the formation of f3A4 aggregates which, in turn, cause damage to growing neurons.
Independent tests showed that although the Appld flies were deficient in fast phototaxis, their defect was not in vision. Since Appld flies were also poor performers in shock reactivity tests that involve escape response induced by a noxious stimulus, we believe that the behavioral deficit is in locomoter reactivity. To demonstrate that the fast phototaxis behavioral deficit is indeed caused by the absence of APPL protein, an Appl minigene constructed using Appl cDNA expressed under the control of a Drosophila heat shock promoter (hsp-Appl+) was used (Fig.
Amyloid Protein Precursor in Development, Aging and Alzheimer’s Disease by C. L. Masters, K. Beyreuther (auth.), C. L. Masters M.D., K. Beyreuther Ph.D., M. Trillet Prof., Y. Christen Ph.D. (eds.)