By Christian Haass
Highlighting the most recent and the main well timed features of Alzheimer's affliction study, this article is going to let scientists in comparable study fields, in addition to physicians operating with Alzheimer's sickness sufferers, to acquire a short and whole assessment of the present cutting-edge in a single of the main fascinating fields in neuroscience learn. prime scientists have contributed articles targeting key advancements during this box. This contains an outline concerning the pathology, the genetics of familial Alzheimer's ailment, proteolytic iteration and aggregation of amyloid -peptide, presenilins, danger components comparable to ApoE, and transgenic animal versions. a few of the most up-to-date advancements in Alzheimer's illness examine, together with the influence of presenilin knock outs on amyloid -peptide iteration, also are integrated.
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Additional resources for Molecular biology of Alzheimer's disease : genes and mechanisms involved in amyloid generation
Sample text
And Flament-Durand, J. (1985) Mise en évidence immunologique de la protéine tau au niveau des lésions de dégénérescence neurofibrillaire de la maladie d’Alzheimer. Arch. Biol. (Bruxelles), 95, 229–235. , and Nunez, J. (1988) Both adult and juvenile tau microtubuleassociated proteins are axon specific in the developing and adult rat cerebellum. Neuroscience, 25, 139–146. A. (1995) Beta-amyloid fibrils induce tau phosphorylation and loss of microtubule binding. Neuron, 14, 879–888. S. (1990) Inhibition of neurite polarity by tau antisense oligonucleotides in primary cerebellar neurons.
This reaction is followed by a series of nearly irreversible rearrangements and subsequent advanced glycation reactions which yield different covalent adducts often termed advanced glycation end-products (AGEs). , 1994). , 1995). , 1995). , 1995). , 1987; for a review see Mori, 1997). Protein chemical analysis of PHF-tau revealed a high ubiquitin content with multi-chained ubiquitin, which usually serves as a degradation signal for a 26S proteasome complex (for a review see Hershko and Ciechanover, 1992).
1985) Mise en évidence immunologique de la protéine tau au niveau des lésions de dégénérescence neurofibrillaire de la maladie d’Alzheimer. Arch. Biol. (Bruxelles), 95, 229–235. , and Nunez, J. (1988) Both adult and juvenile tau microtubuleassociated proteins are axon specific in the developing and adult rat cerebellum. Neuroscience, 25, 139–146. A. (1995) Beta-amyloid fibrils induce tau phosphorylation and loss of microtubule binding. Neuron, 14, 879–888. S. (1990) Inhibition of neurite polarity by tau antisense oligonucleotides in primary cerebellar neurons.