Alzheimer's Disease Related Research Tools
Alzheimer's disease (AD) is the most common form of dementia, a complex neurodegenerative brain disorder characterized by the progressive impairment of cognitive functions, particularly memory, thinking, language, mood, and behavioral issues.
AD is biologically defined by the presence of β-amyloid (Abeta) -containing plaques and tau-containing neurofibrillary tangles. Abeta plaques are formed by the aggregation of beta-amyloid peptides, which are fragments of a larger protein called amyloid precursor protein (APP).
Tau tangles, on the other hand, result from the abnormal phosphorylation and aggregation of tau protein, which is normally involved in maintaining the stability of microtubules within neurons. In Alzheimer's disease, tau protein forms twisted filaments called neurofibrillary tangles.
The accumulation of beta-amyloid plaques and tau tangles initiates a cascade of events that contribute to the progressive neurodegeneration observed in AD. This includes the activation of immune cells (microglia), inflammation, impairment of synaptic connections, and disruption of various signaling pathways in the brain.
As the disease progresses, affected individuals experience a decline in cognitive abilities, memory loss, disorientation, language difficulties, and changes in behavior and personality.
Biological Processes and Targets Related to Alzheimer's Disease
Fig1. Pathophysiology of Alzheimer's disease. (Dhapola, 2021)
| Biological processes | Targets |
| Amyloid-beta plaques formation | APP, Aβ, PSEN1, PSEN2, B2M, Gal-3, AICD, BACE1, RAGE, ADAM, ApoE4, NEP, IDE, GSK-3 |
| Neurofibrillary tangle formation | Tau, NF-kB, TNF-α, ILs, Cdc42, GSK-3β, CDK5, TPK-1, MARK, MAPK, AMPK, Dyrk1A, p53, PAC1R, ERK, CREB, CaMKII |
| Neuroinflammation | TNF-α, TREM2, CD33, NF-κB, CD36, Calhm2, NLRP2, APOE, PGE2, IL-1, IL-2, IL-4, IL-1β, IL-6, IL-10, IFN-γ, TGF-β, SR-A, CR1, ABCA7, KMO, IFN-γ, P2X7R, TLR, CSF1R, miR-155, STAT3, CaSR, ABCA1, BACE1, Aqp4 |
| Oxidative stress | NRF2, NADPH, PGC1α, miRNA-485, SIRT-1, PPAR-α |
| Mitochondrial dysfunction | PGC1α |
| Cholinergic insufficiency | AChE, BuChE, NGF |
| Autophagy dysfunction | PKA, Drp-1, Parkin, mTOR, AMPK, LOX |
| Neurovascular dysfunction | GLUT1, LRP1, P-gp, RAGE, CypA-MMP9 |
| Synapse loss and alterations | NLRP3, RhoA, BDNF, PKCɛ, Jacob, NCAM, MAPK, ERK, NGF, ACSS2, CREB, NMDAR |
| Ferroptosis | NRF2, GPX4, GSS |
| Lipid dyshomeostasis | APOE, HMG-CoA, ACAT1 |
| Genetic risk factor | APOE4, APP, PSEN1, PSEN2 |
Creative Biolabs offers a wide range of cutting-edge research products geared toward the investigation of biological processes underlying Alzheimer's disease. Our products including antibodies, cell lines, proteins & peptides, and assay kits, are among the bio-reagents keenly sought by neuroscience researchers.
Reference
- Dhapola, R.; et al. Recent advances in molecular pathways and therapeutic implications targeting neuroinflammation for Alzheimer's disease. Inflammopharmacology. 2021, 29(6): 1669-1681.
For Research Use Only. Not For Clinical Use.
Target
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