Regeneration_03_06

Regeneration_03_06 - Plasticity and Regeneration Lecture 3...

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Plasticity and Regeneration Lecture 3 Friday, April 1 4 , 200 6 James R. Unnerstall, Ph.D. jru@uic.edu 996-7513 o The inappropriate processing of cellular proteins appears to be a hallmark of many neurodegenerative diseases. This “misprocessing” leads to either loss of function abnormalities or the deposition of the proteins in intra- or extracellular inclusions that can induce inflammatory responses. These localized responses can induce further degeneration. It is unclear, though, whether the degenerative cascade is the result of or the cause of the pathologies which ultimately are only seen post-mortem. o Alzheimer’s disease is characterized by the selective damage to cortical association areas and those wide-projecting systems (such as the basal forebrain cholinergic system or the pontine noradrenergic locus coeruleus system) that modulate cortical function. The deposition of β -amyloid in plaques and tangles is the primary molecular characteristic of the disease. Amyloid fibrils are derived from the amyloid precursor protein which is a notch-like ligand involved in cell-cell differentiation, recognition and survival. Autosomal dominant early- onset forms of AD are characterized by mutations either in the amyloid precursor protein gene itself, or in the processing enzymes and its chaperones (i.e. presenilin). Other mutations, such as the val66 -> met mutation in preBDNF, have been suggested to be risk factors for AD in some forms of late-onset AD. o
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This note was uploaded on 05/02/2008 for the course BIOS 286 taught by Professor Murphy during the Spring '06 term at Ill. Chicago.

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Regeneration_03_06 - Plasticity and Regeneration Lecture 3...

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