Alzheimer

Alzheimer
Alzheimer’s disease (AD), a neurodegenerative disorder, is the most common cause of progressive dementia. Two microscopic characteristics of AD are extracellular amyloid plaques and intracellular neurofibrillary tangles. Amyloid β peptide (Aβ), derived from amyloid precursor protein (APP) by sequential protein cleavage, and other metabolites deposit around neurons and form amyloid plaques, which contribute to the disease’s pathogenesis. The neurofibrillary tangles are formed by the aggregation of phosphorylated tau proteins. Under pathogenic conditions, tau accumulates in dendritic spines and interferes with neurotransmission. The Aβoligomer promotes tau enrichment and facilitates disease progress. read more
- A8190 Semagacestat (LY450139)Summary: γ-secretase inhibitor
- A8200 DAPT (GSI-IX)6 CitationSummary: γ-secretase inhibitor,potent and specific
- A1932 (-)-Huperzine ATarget: NMDA Receptors|AChESummary: NMDA receptor antagonist/AChE inhibitor
- A1038 Amyloid β-Peptide (10-20) (human)Summary: Initiates neurodegeneration in Alzheimer disease
- A1039 Amyloid Beta-peptide (25-35) (human)1 CitationSummary: Functional domain of Aβ
- A1040 Myelin Basic Protein (87-99)Summary: Encephalitogenic peptide
- A1002 Beta-Amyloid (1-11)Summary: Amyloidogenic peptide
- A1003 Amyloid β-Protein (1-15)Summary: Principal component of amyloid
- A1004 Amyloid Precursor C-Terminal PeptideSummary: For beta amyloid generation
- A1005 Beta-Sheet Breaker Peptide iAβ5Summary: Peptide which can inhibit amyloidogenesis