Share these talks and lectures with your colleagues
Invite colleaguesWe noted you are experiencing viewing problems
-
Check with your IT department that JWPlatform, JWPlayer and Amazon AWS & CloudFront are not being blocked by your network. The relevant domains are *.jwplatform.com, *.jwpsrv.com, *.jwpcdn.com, jwpltx.com, jwpsrv.a.ssl.fastly.net, *.amazonaws.com and *.cloudfront.net. The relevant ports are 80 and 443.
-
Check the following talk links to see which ones work correctly:
Auto Mode
HTTP Progressive Download Send us your results from the above test links at access@hstalks.com and we will contact you with further advice on troubleshooting your viewing problems. -
No luck yet? More tips for troubleshooting viewing issues
-
Contact HST Support access@hstalks.com
-
Please review our troubleshooting guide for tips and advice on resolving your viewing problems.
-
For additional help, please don't hesitate to contact HST support access@hstalks.com
We hope you have enjoyed this limited-length demo
This is a limited length demo talk; you may
login
or review methods of
obtaining more access.
Printable Handouts
Navigable Slide Index
- Intro slide
- The usefulness of genetics
- Pathology of diseases
- The beginning of AD research
- The first breakthrough in genetics of AD
- Sequencing families with autosomal AD
- Finding mutations that cause AD
- Amyloid protein precursor
- Effect of mutations on amyloid metabolism
- Alpha and beta pathway of metabolism
- APP 717 and 692 mutations
- The amyloid cascade hypothesis
- Evidence for susceptibility loci on chromosome 14
- FAD locus genetic maps on chromosome 14
- Cloning of a gene bearing missense mutations
- Structure of the presenilin protein - PS1
- A familial AD locus on chromosome 1
- Mutations in PS2
- Mutations in PS line up along helices
- PS1 with the mutations in TM2, TM3 and TM4
- Effect of the mutations
- Is late onset AD caused by related mechanisms?
- Relationship between APP and PS1
- Transgenic models of amyloid deposition
- Presenilin accelerates amyloid pathology
- Tau diseases linked to chromosome 17
- Families with linkage to the FTDP-17 locus
- Taupathologies in families with FTDP
- The microtubule associated protein tau
- Tau is a candidate gene for chromosome 17 FD
- Tau exon 10 3' splice site mutations
- FTDP-17-missense and splicing mutations in tau
- Mice with tangles
- Neurofibrillary tangles formation in transgenic mice
- Gallyas stain
- AD/FTDP-17-pathways to neurodegeneration
- Synuclein
- Alzheimer's diseases
Topics Covered
- Usefulness of genetics in understanding AD
- Pathology of diseases
- Amyloid protein
- Genetic maps
- Mechanism of late onset Alzheimer's
- Role of presenilin in amyloid pathology
- Tau and frontotemporal dementia
- Tau splice site mutations
- Pathways to neurodegeneration
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Hardy, J. (2007, October 1). A molecular understanding of Alzheimer's disease [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved January 19, 2021, from https://hstalks.com/bs/226/.Publication History
Financial Disclosures
- Prof. John Hardy, Consultant: Eisai Speaker's Bureau: Eli Lily Grant/Research Support (Principal Investiqator): MRC/Wellcome Trust
A molecular understanding of Alzheimer's disease
Published on October 1, 2007
42 min