LS2_AlzheimersOutline

LS2_AlzheimersOutline - Shutting Down Alzheimer's Initial...

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Shutting Down Alzheimer’s Initial sign of the disease is often the failure to recall events of the past few days while recollection from long ago remain intact. As the illness progresses, old as well as new memories gradually disappear. Does not only erase information, destroys the hardware of the brain—composed of >100 billion neurons (nerve cells) with 100 trillion connections among them. I. Neurons lost to the disease release acetylcholine (neurotransmitter: chemical communicator). A. Current medications block the enzyme responsible for normal decomposition of acetylcholine. 1. Increase the levels of the depleted neurotransmitter—results in stimulation of neurons and clearer thinking. 2. Become ineffective within six months to a year. B. Mematine , another medication, blocks excessive activity of a different neurotransmitter, glutamate. 1. Slows the cognitive decline in moderate to severe cases. II. The Amyloid Hypothesis A. Two key features of the disease: 1. Plaques and tangles of proteins in the cerebral cortex and limbic system (responsible for higher brain functions). 2. Plaques: deposits found outside neurons; composed of amyloid- β (or A- β : a small protein). 3. Tangles: located inside neurons, axons and dendrites (branching projections); made of filaments of tau (protein). B. Amyloid-cascade hypothesis: both A- β and tau are involved in causing Alzheimer’s, with A- β providing the initial insult. III. A- β : short peptide/protein fragment; derived from amyloid- β precursor protein (or APP: larger protein). A. APP molecules stick through the cellular membrane, with one part inside and the other outside. B. β -secretase and γ -secretase (proteases: protein-cutting enzymes) carve out A- β from APP. C. Production of A- β might be part of a signaling pathway. D. A- β region of APP is inside the membrane; regions of A- β that pass through contain hydrophobic amino acids that cling to one another forming small soluble assemblies. 1. At high enough concentrations, A- β molecules in a test tube assemble into fiberlike structures similar to those found in plaques. 2. Soluble assemblies and A- β fibers are toxic to neurons cultured in Petri dishes; soluble assemblies can interfere with processes critical to learning and memory in mice. IV. Early onset of Alzheimer’s A. Families especially at high risk of Alzheimer’s carry rare genetic mutations that predestine them for the disease at a young age (before 60). 1.
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This note was uploaded on 05/07/2008 for the course LS 2 taught by Professor Pires during the Spring '08 term at UCLA.

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LS2_AlzheimersOutline - Shutting Down Alzheimer's Initial...

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