Registration for a live webinar on 'Innovative Vaccines and Viral Pathogenesis: Insights from Recent Monkeypox (Mpox) Research' is now open.
See webinar detailsWe 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
- Introduction
- Alzheimer's disease (AD)
- Neuropathological lesions associated with AD
- Neurofibrillary tangles
- Beta-amyloid plaques
- Alzheimer amyloid precursor protein (APP)
- APP is cleaved by alpha-secretase
- APP is cleaved by beta-secretase
- Cleavage by gamma-secretase
- Generation of A-beta-42
- Genetic studies
- Genetics of Alzheimer's disease
- APP mutations cluster around secretase sites
- Presenilin and its interactions
- Presenilin (PS1 and PS2)
- Presenilin functions
- FAD-associated presenilins mutations
- Calcium homeostasis
- PS and Ca2+ homeostasis
- FAD-PS1 potentiates calcium release
- Calcium signaling studies
- Ca2+ dyshomeostasis and Alzheimer's disease
- Presenilins have a physiological modulatory role
- A new PS function
- Two new FAD-linked PS2 mutations
- PS2 mutations: M239I and T122R
- FAD-linked PS2 mutations reduce Ca2+ release
- Other FAD linked mutations
- A genetically encoded luminescent Ca2+ sensor
- Effects of PS mutants on cytosolic Ca2+
- Cytosolic Ca2+ changes
- Effects on ER calcium content
- Effects on Golgi calcium content
- Mechanism(s)?
- PS2 mutants increase Ca2+ leak
- PS2 mutants inhibit SERCA pump
- PSs might be multi-functional proteins
- Discordance with the literature?
- An exaggerated Ca2+ response
- Exaggerated Ca2+ release hypothesis for AD
- Does PS affect mitochondria Ca2+ handling
- PS2 expression favors Ca2+ uptake
- PS2 increases ER-mitochondria interaction
- PS2 modulates ER-mitochondria tethering
- A reformulation of the Ca2+ hypothesis for FAD
- References
Topics Covered
- Introduction to Alzheimer's disease
- Morphological and functional features
- Genetic studies
- Presenilin functions and calcium homeostasis
- Calcium dyshomeostasis and FAD
- Modulatory role of presenilin on IP3-evoked Calcium release
- Different effects of PS mutants on intracellular Calcium stores
- A reformulation of the 'Calcium hypothesis' for FAD
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Pizzo, P. (2011, July 27). Ca2+ alterations in familial Alzheimer's disease (FAD) [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved November 21, 2024, from https://doi.org/10.69645/MWJJ2931.Export Citation (RIS)
Publication History
Financial Disclosures
- Dr. Paola Pizzo has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.