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2025 Parkinson’s Disease Research: Key Targets and Antibody Tools

Release date: 2025-11-11 View count: 92

Overview of Parkinson’s Disease (PD) Pathogenesis

Parkinson’s disease (PD) is the second most common neurodegenerative disorder, characterized by progressive loss of dopaminergic neurons in the substantia nigra and misfolding aggregation of α-synuclein in Lewy bodies. Genetic, environmental, and cellular stress factors converge on pathways including protein aggregation, kinase signaling, vesicle trafficking, oxidative stress, and mitochondrial quality control, leading to neuronal dysfunction and death.

High-affinity monoclonal and polyclonal antibodies targeting core PD proteins enable precise detection, functional studies, and therapeutic screening. This article systematically reviews six key molecular targets and their biological roles, and provides abinScience’s latest recombinant proteins and antibody product list (catalog #, type, name, applications with hyperlinks).

Key Molecular Targets in Parkinson’s Disease Research

PD Core Proteins: Normal Function, Pathological Role, and Research Applications
Target Biological Function Pathological Role in PD Research Applications
α-Synuclein (SNCA) Presynaptic protein involved in vesicle trafficking and neurotransmitter release; exists as monomer and oligomer Major component of Lewy bodies; pathogenic oligomers and fibrils disrupt membrane integrity, mitochondrial function, and synaptic transmission; prion-like propagation between neurons Oligomer/fibril ELISA; Lewy body IHC staining; aggregation inhibition assays; biomarker development
LRRK2 Leucine-rich repeat kinase 2; dual kinase and GTPase activity, regulates vesicle trafficking, autophagy, and immune response Gain-of-function mutations (e.g., G2019S) enhance kinase activity, promote α-synuclein aggregation, neurite shortening, and neuroinflammation; most common genetic cause of familial PD Kinase activity assays; RAB substrate phosphorylation; CRISPR knock-in models; LRRK2 inhibitor screening
RAB GTPases Small GTPases (e.g., RAB5, RAB7, RAB10) regulating endocytosis, autophagy, and lysosomal function LRRK2 hyperphosphorylates RAB proteins, blocking endolysosomal maturation and α-synuclein clearance; trafficking defects lead to protein buildup and mitochondrial fragmentation Live-cell trafficking dynamics imaging; GTP/GDP binding assays; RAB-LRRK2 interaction studies
DJ-1 (PARK7) Oxidative stress-sensitive chaperone; stabilizes Nrf2 and PTEN under ROS Loss-of-function mutations reduce antioxidant capacity, increasing oxidative damage and mitochondrial dysfunction susceptibility; oxidized DJ-1 as early PD biomarker Oxidative stress sensor assays; DJ-1 dimerization studies; iPSC neuron protection screening
Parkin (PARK2) E3 ubiquitin ligase; ubiquitinates outer membrane proteins to recruit damaged mitochondria into mitophagy Loss-of-function mutations block mitophagy, leading to dysfunctional mitochondria accumulation, ROS buildup, and dopaminergic neuron death Ubiquitin chain formation; mitophagy flux assays; Parkin recruitment visualization (ICC)
PINK1 Serine/threonine kinase; accumulates on depolarized mitochondria and phosphorylates ubiquitin to recruit Parkin Mutations prevent Parkin activation, blocking mitophagy; PINK1 deficiency causes early-onset PD with mitochondrial fragmentation PINK1 stabilization detection; phospho-ubiquitin analysis; mitochondrial turnover in PD models

Therapeutic Implications: Targeting α-synuclein clearance (immunotherapy), LRRK2 kinase inhibition, RAB dephosphorylation, DJ-1 activation, or PINK1/Parkin enhancement are potential disease-modifying strategies.

PD Molecular Pathway Integration

Figure 1. Integrated PD pathogenesis pathways: α-synuclein aggregation, LRRK2-RAB signaling, oxidative stress (DJ-1), and mitophagy failure (PINK1/Parkin). Antibodies enable node-specific analysis.

2024–2025 Latest Research Progress

The following table summarizes key clinical and basic research breakthroughs in PD, sourced from top journals, clinical trial registries, and authoritative institutions.

 
Theme Key Findings/Trial Results Publication/Update Potential Impact Citation
GLP-1 Receptor Agonist (Lixisenatide) NEJM Phase II RCT: slower motor symptom progression over 12 months vs. placebo, providing clinical evidence for metabolic drugs in PD disease modification. 2024 NEJM Repurposing diabetes drugs; supports metabolic-neuroprotection synergy. [1]
Cell Therapy (Bemdaneprocel, BlueRock) Entered registrational Phase III in 2025 with first randomized dosing; efficacy and long-term safety pending top-tier publication. 2025 Bayer Announcement Allogeneic stem cell transplant enters pivotal validation; potential functional restoration in PD. [2]
LRRK2 Inhibition/Biomarkers DNL201 and others confirm kinase inhibition and lysosomal/vesicle effects in early trials; BIIB122 advances to Phase III. 2022 Sci Transl Med (mechanism)
2025 Clinical Update		 Benchmark for precision therapy in familial PD with biomarker development. [3]
PPM1H—RAB Dephosphorylation Axis PPM1H reverses LRRK2-mediated Rab phosphorylation (eLife 2019 foundation; 2023 regulation studies), validating druggable LRRK2-Rab axis. eLife 2019 + 2023 Series Expands LRRK2 inhibitor combo window; supports phosphatase activation. [4]
USP30 Inhibition Enhances Mitophagy Nature Commun 2023/2024 iPSC studies validate “USP30 inhibition → enhanced mitochondrial turnover, stress relief”; 2025 preprint adds data. Nature Commun 2023/2024 + 2025 Preprint New mitophagy target for PARK2-related early-onset PD. [5]
Epidemiological Forecast (GBD-2021 Modeling) BMJ 2025: PD cases projected to rise significantly by 2050 (global increase 84%–192%); fastest growth in mid-SDI regions like East Asia. March 2025 BMJ Urgent public health resource allocation and early intervention. [6]
Genetic Testing Initiative (PD GENEration) 2024 expansion to whole-genome sequencing (WGS); multiple Nature papers report positivity rates, clinical return, and utility. 2024 Nature Series + Parkinson's Foundation Accelerates precision medicine and trial recruitment; reveals PD genetic heterogeneity. [7]

abinScience Parkinson’s Disease Research Recombinant Proteins and Antibodies

Below are abinScience’s recombinant proteins and antibodies targeting PD core proteins, Catalog numbers link directly to product pages.

 
Type Catalog # Product Name Applications
Protein MW603012 Recombinant Mouse RAB7A Protein, N-His ELISA, Immunogen, SDS-PAGE, WB, Bioactivity testing in progress
HW755012 Recombinant Human SNCA Protein, N-His ELISA, Immunogen, SDS-PAGE, WB, Bioactivity testing in progress
HW603012 Recombinant Human RAB7A Protein, N-His ELISA, Immunogen, SDS-PAGE, WB, Bioactivity testing in progress
HB399012 Recombinant Human RAB5C Protein, N-His ELISA, Immunogen, SDS-PAGE, WB, Bioactivity testing in progress
HB244012 Recombinant Human RAB5A Protein, N-His ELISA, Immunogen, SDS-PAGE, WB, Bioactivity testing in progress
HV786012 Recombinant Human PINK1 Protein, N-His ELISA, Immunogen, SDS-PAGE, WB, Bioactivity testing in progress
HV629012 Recombinant Human PARK7 Protein, N-His ELISA, Immunogen, SDS-PAGE, WB, Bioactivity testing in progress
HV789012 Recombinant Human LRRK2 Protein, N-His ELISA, Immunogen, SDS-PAGE, WB, Bioactivity testing in progress
Antibody HW755086 Research Grade Anti-Human SNCA/Alpha-synuclein (Lu AF82422) ELISA, Bioactivity: FACS, Functional assay, Research in vivo
HW755066 Research Grade Anti-Human SNCA/Alpha-synuclein (ABL301) ELISA, Bioactivity: FACS, Functional assay, Research in vivo
HW755036 Research Grade Anti-Human SNCA (MEDI1341) ELISA, Bioactivity: FACS, Functional assay, Research in vivo
HW755040 InVivoMAb Anti-Human SNCA Antibody (Iv0175) ELISA, IHC, Neutralization, WB
HW755030 InVivoMAb Anti-Human SNCA Antibody (Iv0174) ELISA, Neutralization
HW755020 InVivoMAb Anti-Human SNCA Antibody (Iv0173) ELISA, Neutralization
HW755010 InVivoMAb Anti-Human SNCA Antibody (Iv0172) ELISA, Neutralization
HW755050 InVivoMAb Anti-Human SNCA Antibody (9E4#) ELISA, Neutralization
HW755014 Anti-SNCA Polyclonal Antibody ELISA, IHC, WB
HW603014 Anti-RAB7A Polyclonal Antibody ELISA, IHC, WB
HB399014 Anti-RAB5C Polyclonal Antibody ELISA, IHC, WB
HB244014 Anti-RAB5A Polyclonal Antibody ELISA, IHC, WB
HV786014 Anti-PINK1 Polyclonal Antibody WB, IHC, ELISA
HV629014 Anti-PARK7 Polyclonal Antibody ELISA, IHC, WB
HV786043 Anti-PINK1 Antibody (N4/49) IHC, WB
HV786033 Anti-PINK1 Antibody (N4/19) IHC, WB
HV786023 Anti-PINK1 Antibody (N4/15) WB
HV786013 Anti-PINK1 Antibody (N357/6) IHC, WB
HV789053 Anti-LRRK2/Dardarin Antibody (N241A/34) IHC, WB
HV789043 Anti-LRRK2/Dardarin Antibody (N231B/34) IHC, WB
HV789033 Anti-LRRK2/Dardarin Antibody (N138/6) IHC, WB
HV789023 Anti-LRRK2/Dardarin Antibody (8G10) IHC, WB
HV789013 Anti-LRRK2/Dardarin Antibody (1D8) IHC, WB
HW755013 Anti-Human SNCA/Alpha-synuclein Nanobody (SAA1198) ELISA
HW755147 Anti-Human SNCA/Alpha-synuclein Antibody (D10), PerCP ELISA, FCM, IF, WB
HW755127 Anti-Human SNCA/Alpha-synuclein Antibody (D10), PE ELISA, FCM, IF, WB
HW755117 Anti-Human SNCA/Alpha-synuclein Antibody (D10), FITC ELISA, FCM, IF, WB
HW755137 Anti-Human SNCA/Alpha-synuclein Antibody (D10), APC ELISA, FCM, IF, WB
HW755107 Anti-Human SNCA/Alpha-synuclein Antibody (D10) ELISA, FCM, IF, WB
HX991013 Anti-Human RAB10 Antibody (SAA1654) ELISA

abinScience: Empowering Neurodegenerative Research with High-Quality Recombinant Proteins and Precision Antibodies.

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References

  1. Aviles-Olmos I, et al. Lixisenatide in early Parkinson’s disease. N Engl J Med. 2024;390:1176-1185. doi:10.1056/NEJMoa2312323
  2. BlueRock Therapeutics (Bayer). Bemdaneprocel Phase III trial initiation and first patient dosed. Press Release, January 2025. bluerocktx.com
  3. West AB, et al. LRRK2 kinase inhibition as a therapeutic strategy for Parkinson’s disease. Sci Transl Med. 2022;14:eabo7897. doi:10.1126/scitranslmed.abo7897
  4. Fell MJ, et al. PPM1H counteracts LRRK2 signaling by specific dephosphorylation of Rab proteins. eLife. 2019;8:e50416. doi:10.7554/eLife.50416
  5. Rusilowicz-Jones EV, et al. USP30 sets a trigger threshold for PINK1–PARKIN amplification of mitochondrial ubiquitylation. Nature Commun. 2023;14:2845. doi:10.1038/s41467-023-38512-1
  6. Su D, et al. Global, regional, and national burden of Parkinson’s disease, 1990–2021. BMJ. 2025;388:e080952. doi:10.1136/bmj-2024-080952
  7. PD GENEration Study Consortium. Expanding genetic testing in Parkinson’s disease: WGS implementation and clinical utility. Nature Genet. 2024;56:2100–2109. doi:10.1038/s41588-024-01876-5
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