MCDB 4777/5777 Molecular Neurobiology Lecture 38 Alzheimer s Disease

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1 MCDB 4777/5777 Molecular Neurobiology Lecture 38 Alzheimer s Disease

2 Outline of Today s Lecture Why is Alzheimer s disease a problem? What is Alzheimer s Disease? What causes Alzheimer s disease? How can we test whether something causes the disease? How can we try to interfere with the cause? (i.e. develop a drug to treat the disease) How can we quickly and safely test whether the drug may work? Kevin Jones

3 Learning Goals for Lecture Explain how genes, molecules, cells, and neural circuits interact in the generation of several neurodegenerative disorders. a. Recognize symptoms of major neurodegenerative disorders b. Apply understanding of functional neural anatomy to predict the location of degeneration, based on symptoms. c. Identify uses of forward and reverse genetics in defining the molecular basis for neurodegenerative disorders. d. Recognize gene mutations associated with major neurodegenerative disorders and the effects of those mutations on proteins they encode e. Describe how a gene mutation may lead to molecular mechanisms of pathogenesis in neurodegenerative disorders. f. Predict potential strategies for developing successful treatments for different neurodegenerative disorders. g. Use information about the molecular basis of neurodegeneration to distinguish between treatments that affect symptoms versus influence the underlying cause of a neurodegenerative disorder. h. Outline the steps of bringing a logical treatment for a neurodegenerative disorder to clinical trial

4 Alzheimer s Disease- an epidemic in progress

5 progression Plaques and tangles (shown in the blue-shaded areas) tend to spread through the cortex in a predictable pattern as Alzheimer s disease progresses. The rate of progression varies greatly. People with Alzheimer s live an average of eight years, but some people may survive up to 20 years. The course of the disease depends in part on age at diagnosis and whether a person has other health conditions. Earliest Alzheimer's changes may begin 20 years or more before diagnosis. Mild to moderate Alzheimer stages generally last from 2-10 years. Severe Alzheimer s may last from 1-5 years. From

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7 What Causes Alzheimer s Disease? Alois Alzheimer, a German doctor, published a paper in 1907 describing the case of a woman having dementia. After she died, he had autopsied her and found deposits in her brain. The deposits are called Amyloid Plaques and Neurofibrillary Tangles Amyloid Plaque Neurofibrillary Tangles

8 The genetics of Early-Onset Familial Alzheimer s Disease Mutations were found in the following genes: Presenilin-1 Presenilin-2 The Presenilins are membrane proteins involved in proteolytic processingthought to be γ-secretase components Amyloid Precursor Protein (βapp) This is the protein that is processed to give the β- amyloid peptide βapp mutations account for less than 0.1% of total AD cases but have virtually complete penetrance

9 Proteolytic Processing of the Amyloid Precursor Protein Generates β-amyloid peptide Processing Pathways: 1- α + γ secretases gives p3 peptide 2- β + γ secretases gives β40 peptide 3- β + γ secretases gives β42 peptide- insoluble Presenilin-1 is necessary for γ secretase activity!

10 Mutations in the β-amyloid Precursor Gene Donald L. Price, * Sangram S. Sisodia, David R. Borchelt Science Volume 282, Number 5391, Issue of 6 Nov 1998, pp

11 The Amyloid Hypothesis Production of Aβ (especially the relatively insoluble Aβ42) Formation of extracellular deposits Neuron atrophy and death =Alzheimer s disease According to this hypothesis, FAD mutations enhance the production of Aβ42

12 A current view of AD progression Preclinical phase- pathological changes occurring in cells not yet apparent in neurological testing- biomarkers can detect with false positives and negatives Mild Cognitive Impairment (MCI)- neurological symptoms apparent, imaging and biomarkers can detect alterations more reliably (CSF low Aβ high tau), plaques apparent but not strongly correlated w/ degree of impairment Dementia- profound neurological symptoms, rapid decline, not associated with pronounced increase in plaque burden but tangles more apparent

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14 Why care about biomarkers like this? A- the graphs are pretty so it makes lecture more entertaining B- they allow an exact diagnosis C- they help with diagnosis and could prove useful in treating early D- they allow promptly institutionalizing individuals with Alzheimer s

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16 The Amyloid Hypothesis Selkoe, 2002 Science

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18 Current Alzheimer s Therapeutics Cholinesterase Inhibitors The U.S. Food and Drug Administration (FDA) has approved two classes of drugs to treat cognitive symptoms of Alzheimer s disease. The first Alzheimer medications to be approved were cholinesterase inhibitors: Three of these drugs are commonly prescribed: donepezil (Aricept ), approved in 1996 rivastigmine (Exelon ), approved in 2000 galantamine (approved in 2001 under the trade name Reminyl and renamed Razadyne in 2005). Memantine Memantine (Namenda ) is a drug approved in October 2003 by the FDA for treatment of moderate to severe Alzheimer s disease. Memantine is classified as an uncompetitive low-to-moderate affinity N-methyl-D-aspartate (NMDA) receptor antagonist, the first Alzheimer drug of this type approved in the United States. Source:

19 How does the use of acetylcholinesterase inhibitors to treat Alzheimer s disease relate to the mechanism you think causes the disease? A. By enhancing acetylcholine function, it should enhance the activity of circuits and make the neurons more resistant to damage B. By prolonging the existence of acetylcholine, it has more of a chance to exert its neurotrophic effects C. By enhancing the activity of acetylcholinesterase, it can degrade Aβ oligomers found in the extracellular space D. Acetylcholine can promote the formation of new excitatory synapses, helping replace those that have been lost E. Acetylcholine has no apparent relevance to the mechanisms I am thinking of

20 wikipedia.org

21 Alz.org

22 The genetics of Alzheimer s Disease Susceptibility genes- Having one ApoE4 allele- ~5x increase in risk Having 2 ApoE4 alleles- ~15x increase in risk 3 alleles at this locus (ApoE2, ApoE3, ApoE4) ApoE4 is ~15% frequency in Caucasians ApoE protein important in lipid and protein transport, cardiovascular disease somehow relevant to amyloid deposition? SORL1- amyloid processing?- association study published 1/07

23 Do you want to know your ApoE genotype? A- yes B- no, never C- not now, maybe when I reach old age

24 Meta-analysis of 74,046 individuals identifies 11 new susceptibility loci for Alzheimer's disease

25 The SORL1 protein directs APP into recycling endosomes, which shuttle it to the cell membrane. But when SORL1 is absent, APP goes instead to the late endosomes, where the enzymes BACE and PS1 snip out neurotoxic amyloid. Science 19 Jan 2007 p.314

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