MOA of aSyn spreading tail, Antibodies to aSyn (matrix + per-antibody host/Species/epitope), Vaikath 2019 #1599 antibody fragment map, Astrocytic aSyn (Aflaki 2020 GD1/GD2 iAstrocytes), CSF & Blood Total aSyn level start

Antibodies to aSyn

Pathologic conversionPathological aggregation
monomerictetramerPhosphorylated a-synMisfolded monomerB-pleated sheetinsolubleOligomeric (still soluble)
((Wang et al., 2016))
protofibril(insoluble amyloid-like) fibrilLewy bodiesTotal a-syn
Antibody(20200414) ADx Neurosciences, TV Q3 FY2020, CS : Q42020,
• 기존 : anti-pS129 a-syn polyclonal antibody (Santa Cruz)
(Waxman, 2008 #535) Syn505, Syn506 and Syn514 recognize conformational variants of α-synThioflavin-s staining (antibody는 아니지만) • (20200414) ADx Neurosciences, TV Q4 FY2020, CS : Q3 FY2021,
A-mouse anti-α-syn fibrils/oligomers (O2; [43]),
mouse anti-α-syn fibrils/oligomers (O2; [43])

mouse anti α-syn fibrils (F2; [43])
-current Abs can't distinguish physiological (HC) between pathological species (PD pts)

Per-antibody host / Species / epitope

AntibodyhostSpeciesepitopenote
A11, AB9234, Merck Milliporeantibodies specifically raised against oligomeric forms of a-syn but bind to Aβ as well
OC, AB2286, Merck Milliporeanti-amyloid fibril antibody (Aβ as well)
SNL1Murine and human, but (Yazawa, 2005 #1440) only mouse aSyn)PNAS. 2009. 106: 20051 SNL1 and SNL4: pan aSyn antibodies
SNL4PNAS. 2009. 106: 20051 SNL1 and SNL4: pan aSyn antibodies
LB509specific for human115-122
C20human, mice, rat (alzforum),Cterm of aSyn
81AhumanOnly phosphorylated aSyn
Syn-1human91-99
Syn03
Syn 202aa 130-140 (Giasson, 1999 #2823)Human aSyn (aSyn propagation suppressor slide)
Syn204specific for humanAa 87-110 (Giasson, 1999 #2823) shares aa 87-109
Syn 205aa 130-140 (Giasson, 1999 #2823)
Syn 208Aa 87-110 (Giasson, 1999 #2823)
Syn211Only human,121-125PNAS. 2009. 106: 20051 Syn506 and Syn211 mostly recognized α-syn antibodies
Syn303
Syn506BD Biosciencesonly recognized aa residues 125-129 of α-syn (non-p form)Used in NURR's Atuka study
EP1536Y (=ab51253)HUMAN & mouse & rat
610787 (BD Biosciences)Pan aSyn
Syn1150only recognized aa residues 125-129 of α-syn (non-p form)
D37A6Only mouse
MJFR1Only human
Syn-O2Majbour 2016: specifically recognizes early soluble "oligomers" and late aggregates "amyloid fibrils" of α-syn (Fig. 1a), and has a high binding affinity for o-α-syn species (apparent KD value of ~5×10⁻¹¹ M) [24]. It exclusively detects o-α-syn aggregates (amyloid fibrils and soluble oligomers) without cross-reactivity with monomers or fibrils in conjunction with Nells but Otake- Five years ago I have tried to detect RT QuIC reaction product in western blotting using one of Du I could not any signal
MJFR-14-6-4-2(Vaxxinnity AD/PD 2024 update)
2A1(Majbour 2021) a conformation specific antibody that specifically recognizes α-syn aggregates both full-length (1-140 aa) and C-terminally truncated (1-1...)
3G7(Majbour 2021) 3G7, a conformation specific antibody, recognizes a wide range of α-syn forms including C-terminal truncated forms (Fig. S2; ?)
4D6Full length aSyn, cross-reactive with paSyn
5C2mouse61-90
5G4):5G4 specifically recognizes aa 47-52 in B-sheet form of α-syn oligomers, do not capture normal oligomeric αSyn
x122 a-syn antibody(A15127A from BioLegend)on the a-syn (1-121)
https://www.biolegend.com/ja-jp/products/purified-anti-alpha-syn-c-terminal-truncated-a-122-13986?GroupID=BLG11651
may recognize neo-epitope which is not exist in full length a-syn (but a little bit skeptical)

(Vaikath, 2019 #1599) list and summary of antibodies with (conformation-specificity) in table 1

A: aSyn fragment map labels visible: A30P, A53T, NAC, Pan-Syn (1-95 region highlighted), N-1&2 (1-61), NAC-1&2 (61-95), Syn-1, Hu-Syn (95-140), NACP-C, 140

above Li, 2005 #2044

Astrocytic aSyn

Astrocytic inclusions of αSyn are invariant features in PD and DLB but observed less frequently in MSA (Sorrotion, 2019 #1138).

mechanism (when astrocyte don’t express asyn)

  • {Aflaki, 2020 #1141} in Gaucher iPS-derived astrocytes,
    • ↓ glucerebrosidase activity (GD1 iAstrocytes showed the expected reduction in GCase activity (~35% of control), whereas GD2 iAstrocytes had severely deficient (<5% of control) GCase activity (Fig. 2C)
    • accumulate glucoslyceramide, upregulated GFAP and several astrocyte astrogliosis
  • iAstrocytes from the subjects with GD1 with a parkinsonian phenotype
  • two lines generated from the subject with GD2 had 3.5 and 5.6 fold elevations in GlcCer than control iAstrocytes. Cells from two lines generated from the subject with GD2 had 3.5 and 5.6 fold elevations in GlcCer level compared to those from an infant control (Fig. 2G).
    • GlcSph levels were significantly elevated in GD2 iAstrocytes (10-20 fold) (Fig. 2E)
  • Excessive α-syn from neurons is taken up by astrocytes and moved into lysosomes (iDA neurons 과 co culture 실험 통해서)
  • Cathepsin D activity is low in iAstrocytes from Parkinson’s disease and GD2 patients

CSF & Blood (a-syn)

[Total aSyn level]

  • Hansson 2014, Skåne University Hospital, Sweden: 60 ng/L, ↓8% (a new)
  • Majbour 2021: DenoPa 826 pg/Ml, ↓8%, in-house
  • Majbour 2016, VUMC, : 1.5 ng/mL, ↓19% (p<0.05), in-house
  • van Steenoven, 2018, VUMC, 1.5 ng/mL, ↓22%, the same assay as M
  • {Schirinzi, 2019 #615}, Italy, 1,000 pg/mL, ↓33% p<0.05, ELISA kits (Covance=BioLegend), ~1.5 ng
  • {Baek, 2021 #2734} ppmi, ELISA kits (Covance=BioLegend), ~1.5 ng