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and I saw some time ago was that ACT antibodies sometimes stained neuronal cell bodies. Nienwen
Ma J. and Potter H. Alzheimer presenilins in the nuclear membrane, interphase kinetochores, and
protein and ubiquitin-B in Alzheimer's and Down's syndrome patients. Science 1998 Jan 9;279
so. The neurons are alive! Carl Cotman: Perhaps a very long time. This is the point: There are DNA and
proteins, in normal and Alzheimer states; and Pin1 and the paradigm of phosphorylation-dependent prolyl
inducible system, the length of time of induction and level of induction also provides varying results. Our
Dennis Selkoe, Dean Hartley, and William Klein led this live discussion on 17 February 2000.
huntingtin is turned off and the inclusions go away. Soshi: World Alzheimer Congress meeting data suggest
a chance to address. Imaizumi: I think [they are] differences of treatment of stressors, dose and time
Alzheimer's neuropathology and is not simply a supporting actor. If this were true, one would expect that
transplantation therapy for neurodegenerative diseases such as Parkinson's, Alzheimer's, and
a difference in TUNEL+ cells between PS1-KO and control mice. But it remains possible that at other time
Alzheimer's, most Ab is degraded and does not accumulate. Larry Goldstein: Interesting. I'll have to
Harvard Medical School and we model neurodegenerative diseases, including Alzheimer's disease and
2000;59(9):768-773. Abstract Haglund M, Englund E. Cerebral amyloid angiopathy, white matter lesions and Alzheimer
Have a topic idea for a webinar? We would love to hear it. Send an email to webinars [at] alzforum [dot] org.
