about
Alzheimer's disease-like APP processing in wild-type mice identifies synaptic defects as initial steps of disease progression.Cholesterol 24-hydroxylase defect is implicated in memory impairments associated with Alzheimer-like Tau pathology.Viral gene transfer of APPsα rescues synaptic failure in an Alzheimer's disease mouse model.CYP46A1 inhibition, brain cholesterol accumulation and neurodegeneration pave the way for Alzheimer's disease.The mechanisms of cell death in focal cerebral ischemia highlight neuroprotective perspectives by anti-caspase therapy.PTD-XIAP protects against cerebral ischemia by anti-apoptotic and transcriptional regulatory mechanisms.Activation of proinflammatory caspases by cathepsin B in focal cerebral ischemia
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Q27301267-0A559684-29BC-4211-BC1A-0E7E48A0CE85Q34044871-A10EB6FC-159E-4058-868E-1948C5FD97E8Q40354888-7A2C8031-70A2-42C1-97CC-8F232AB6866FQ41614229-608DB83B-C095-444F-87B8-EF6C430C35FAQ48174301-61EB3ECB-7782-4786-B7B6-F3D6625C38C0Q51302929-447A936F-72E5-45D5-9470-DC36440C81BBQ81012298-B7F557B1-5842-4BFC-B3D9-3E6175939036
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description
researcher ORCID ID = 0000-0002-1147-8611
@en
wetenschapper
@nl
name
Jérome Braudeau
@ast
Jérome Braudeau
@en
Jérome Braudeau
@es
Jérome Braudeau
@nl
type
label
Jérome Braudeau
@ast
Jérome Braudeau
@en
Jérome Braudeau
@es
Jérome Braudeau
@nl
prefLabel
Jérome Braudeau
@ast
Jérome Braudeau
@en
Jérome Braudeau
@es
Jérome Braudeau
@nl
P106
P1153
6508202488
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P496
0000-0002-1147-8611