Alzheimer's disease

Alzheimer's disease is the most common neurodegenerative disorder, with β-amyloid deposition and pathological tau phosphorylation as hallmark features. We provide antibodies and small-molecule tools spanning Aβ, tau, the secretase axis, and neuroinflammation to support mechanistic, biomarker, and therapeutic research.

Focus areas: amyloid cascade, tau propagation, synaptic loss, glial reactivity, proteostasis, and metabolic/vascular contributions

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Hot topics & directions

  • Aβ production vs clearance: APP processing, secretase activity, and degrading enzymes (e.g., NEP/IDE) jointly explaining plaques.
  • Tau pathology & spreading: Seeds, PTM landscapes, and trans-cellular propagation—model-dependent reproducibility.
  • Synaptic & circuit function: Pre/post-synaptic markers vs electrophysiology aligned with disease staging.
  • Neuroimmune & vascular factors: Microglia/TREM2, complement cascades, and BBB integrity as convergent modifiers.

Related targets

Amyloid cascade
APP, BACE1, ADAM10, PSEN1/2, NCSTN, APH1A/B, PEN2, Aβ42/40
Tau & cytoskeletal regulation
MAPT, GSK3β, CDK5, PP2A regulatory subunits (context-dependent)
Lipid & innate immune genetics
APOE, TREM2, CD33, MS4A, CLU / APOJ, INPP5D
Synapse & clearance pathways
LRP1, PICALM, BIN1, VCP/p97–proteasome–autophagy crosstalk (model-dependent)

Key signaling pathways

  1. APP → BACE1/ADAM10 → CTFs → γ-secretase → Aβ
    Competition between amyloidogenic vs non-amyloid (α-) processing is a central mechanistic axis.
  2. GSK3β / CDK5 → tau hyperphosphorylation
    Multi-site phosphorylation pairs with aggregation/seeded propagation assays.
  3. Complement & microglial sensing
    Synaptic pruning vs inflammatory amplification—separate causality from association.
  4. mTOR–autophagy–lysosome
    Proteostasis stress often couples to mitochondrial strain; match readouts to time scales.

Tool compounds (research use)

Commonly used for mechanistic studies; follow your lab SOP, compound datasheets, and ethics approvals.

CompoundTargets / pathwaysExperimental notes
DAPTγ-secretase complex (watch Notch-related off-targets)Blocks Aβ production / studies APP processing; mind Notch-related toxicity in vivo/long runs.
LY-411575γ-secretasePotent tool; use tight dose windows and mechanistic controls vs other GSIs.
Compound Eγ-secretaseClassic in vitro tool; mind batch solubility and vehicle controls.
CHIR99021GSK3β (also GSK3α; concentration-dependent)Common for tau hyperphosphorylation readouts; pair total protein + multi-site phospho antibodies.
RapamycinmTORC1 (FKBP12–Raptor)Autophagy/proteostasis studies; chronic dosing may engage mTORC2 feedback.
MG132ProteasomeUPS-dependent stability of APP/tau fragments; high cytotoxicity—window doses tightly.
FK506 (Tacrolimus)CalcineurinOccasionally used in synaptic plasticity/phosphatase axes; mind immunosuppression/off-targets.