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

PNUTS

Urokinase

SOD

TREM1

UBE2K

IBA1

TLR9

Tubulin β 3

MUC2

PIN1

ERK1/ERK2

Neurofilament L

TMP21

TREM2

FUS

CD282

S100A8

VWF

NF-kB p65

Vimentin

Amyloid beta

AACT

DYSF

GSK-3

FE65

TRPM4

Cleaved Caspase-3

CD29

Munc18-1

VPS35

UCP1

VAP1