All Comments by Andre Delacourte
- Presenilin Loss of Function—Plan B for AD?
- Modulation of synaptic plasticity and Tau phosphorylation by wild-type and mutant presenilin1.
- The presenilin hypothesis of Alzheimer's disease: evidence for a loss-of-function pathogenic mechanism.
- Collective Thought at Its Best: Let’s Contemplate the Centennial
- BACE1 inhibition reduces endogenous Abeta and alters APP processing in wild-type mice.
- Neuroprotective effects of (-)-epigallocatechin-3-gallate in a transgenic mouse model of amyotrophic lateral sclerosis.
- An inhibitor of tau hyperphosphorylation prevents severe motor impairments in tau transgenic mice.
- An immunohistochemical study of cases of sporadic and inherited frontotemporal lobar degeneration using 3R- and 4R-specific tau monoclonal antibodies.
- Mechanisms of action of green tea catechins, with a focus on ischemia-induced neurodegeneration.
- Reduction of Abeta levels in the Sprague Dawley rat after oral administration of the functional gamma-secretase inhibitor, DAPT: a novel non-transgenic model for Abeta production inhibitors.
- Therapeutic effects of PKC activators in Alzheimer's disease transgenic mice.
- APP locus duplication causes autosomal dominant early-onset Alzheimer disease with cerebral amyloid angiopathy.
- Suppression of cyclin-dependent kinase 5 activation by amyloid precursor protein: a novel excitoprotective mechanism involving modulation of tau phosphorylation.
- Beta-site APP cleaving enzyme 1 (BACE1) is increased in remaining neurons in Alzheimer's disease brains.
- Progressive neuronal loss and behavioral impairments of transgenic C57BL/6 inbred mice expressing the carboxy terminus of amyloid precursor protein.