α-Synuclein and Lewy pathology in Parkinson’s disease – Kalia and Kalia

Table 1. Relationships between genetic forms of Parkinson’s disease and Lewy pathology

geneproteinprotein present within Lewy bodiesLewy bodies associated with disease
Monogenic Parkinson's disease
Autosomal dominant
SNCAα-Synuclein++
LRRK2Leucine-rich repeat kinase 2++/-
VPS35Vacuolar protein sorting 35-?
EIF4G1Eukaryotic translation initiation factor 4γ 1+/-+
DNAJC13Receptor-mediated endocytosis 8 (REM-8)+/-+
CHCHD2Coiled-coil-helix-coiled-coil helix domain containing 2??
Autosomal recessive
ParkinParkin++/-
PINK1PTEN-induced putative kinase 1++
DJ-1DJ-1+?
Other genetic parkinsonism
Autosomal dominant
C9ORF72Dipeptide repeat proteins?+
SCA2Ataxin 2?+
SCA3Ataxin 3??
Autosomal recessive
ATP13A2ATP13A2+-
DNAJC6Auxilin??
FBXO7F-box protein 7+?
GBAGlucocerebrosidase++
PANK2Pantothenate kinase 2?-
PLA2G6Phospholipase A2 group VI++
SLC18A2Vesicular monoamine transporter 2 (VMAT2)+?
SPG11Spatacsin+?
SYNJ1Synaptojanin 1??
Other
POLG1Polymerase γ 1?+/-
RAB39BRab protein 39B?+
22q11.2 microdeletion??+/-

이들 Mutation 이 coding 하는 protein 이 LB 내에 발견되는가?

o parkinsonism, LRRK2 has been found to localize to Lewy bodies in Parkinson’s disease[31] but not VPS35 [32]. EIF4G1 or DNAJC13 immunoreactivity in Lewy bodies has only been examined in postmortem samples from patients with Parkinson’s disease with corresponding gene mutations; less than 50% of Lewy bodies were found to be immunoreactive for DNAJC13 [33] and most were nonimmunoreactive for EIF4G1 [34]. Among the proteins associated with autosomal recessive parkinsonism, parkin, PINK1, DJ-1 (reviewed in [24]), ATP13A2 [35], and FBXO7 [36] have all been reported to localize to Lewy bodies.

GBA

PD w GBA mutations 환자PD w/o GBA mutations 환자
GBA가 LB내에 있는 확률75%<10%

Supplement: Positive vs Negative

Lysosomal function

contextpositivenegative
in vitroKO `{Osellame, 2013 #534}` Mixed mid-brain cultures of cortical neurons and astro-cytes)CBE (Cleeter, SH)
KD (Mazzulli)CBE (Dermen, SH)
KO `{Bae, 2014 #610}` (Fig 5)CBE (Dermen, PC)
in vivo`{Rocha, 2015 #1253}` CBE (100mg/kg, 28 d) → ↑ cathepsin D (protein), ↑ LAMP2A, ↑ LC3-II, (P62 only increasing trend)

a-syn

contextpositivenegative
in vitroCBE (Manning-Bog,SH)CBE (Cullen, PC12)
CBE (Cleeter, SH)CBE (Dermen, SH)
KD (Mazzulli)CBE (Dermen, PC)
RNAi `({Zurbruegg, 2019 #687}, SH-SY5Y cells`CBE `{Zurbruegg, 2019 #687}`, SH SY5Y cells and rat primary cortical cultures
`{Henderson, 2020 #1233}` In PFF-treated mice embryonic (hippocampal능) neurons: CBE → ↑ pS129-aSyn (fig3 f,g,l,i)`{Henderson, 2020 #1233}` In mice embryonic (hippocampal능) neurons: CBE → = pS129-aSyn
in vivo`(D409Vgba KI mouse, Cullen)` 12month homoz hippocampus에서만 올라가고, 12month homoz brain stem, 12month hetero, 12 week homo에선 안 올라갔음.
2013 Osellame: ↑ Oligomeric aSyn in KO mouse (K14-Inl/Inl Mice)
Homoz (mid brain, Osellame),, monomeric aSyn 은 no change
KO (K14-Inl/Inl) mouse Heteroz (midbrain, Osellame)
L444P and R463C point mutation mouse(Ginns,) in Striatum
(hetero는 안 쓰인 것 같음)
CBE (Manning-Bog,midbrain)
CBE (Ginns) in SN & Straitum
CBE 100mg, 28 d (Rocha) → ↑ proteinase-K resistant a-syn aggregates
`{Papadopoulos, 2018 #1273}` CBE+A53T mice: ↑ aSyn soluble monomer in midbrain, striatum aSyn oligomer, (but no change in p-aSyn,), see additional details of Asyn different species and different regions.`{Henderson, 2020 #1233}` In PFF-treated mice: CBE → ① = dopaminergic neuronal loss in SN (fig 5F), ② GCase inhibition does not induce aggregation of a-syn but rather induces mild neuronal spheroids recognized by 81A, which can cross-react with neurofilament ③ 거의, = aSyn spread (to cortex) fig 6B

Synapse

contextpositivenegative
in vivo`{Rocha, 2015 #1253}` CBE (100mg/kg, 28 d) → c1q, SNAP-25, Synaptophysin, synaptoagmin, synapsin, PSD-95

총정리 GBA protein & activity POSTMORTEM

Activity: hetero only 에선 kurzawa가 유일. GlcSph Blood: 에서 단독으로 본 것 없잖아!? (2017 Guedes에선 galactosylsph와의 sum), 이거 못 보나 Sato에게 물어보자.

sampleGBA proteinGBA activityGlcCerGlcSphCathepsin D proteinCathepsin D activityLIMP2LAMP2LC3
Brain (Li, 2019 #745) In supplement
(Gundner et al. 2019, PMID 30236861)
(Gegg et al. 2012, PMID 23034917)
(Choi et al. 2011, PMID),
(Kurzawa-Akanbi, 2012 #577)
In supplement
(Moors, 2019 #644)
(Li, 2019 #745)
(Gundner et al. 2019, PMID 30236861)
(Gegg et al. 2012, PMID 23034917)
(Choi et al. 2011, PMID),
(Kurzawa-Akanbi, 2012 #577)
(Gegg et al. 2012, PMID 23034917 but =
(Kurzawa-Akanbi, 2012 #577) but =
In supplement
(Moors, 2019 #644)
(Kurzawa-Akanbi, 2012 #577) ↓
(Gegg et al. 2012, PMID 23034917 but =
CSF Schondorf et al. 2014, PMID 24905578) In supplement
(Parnetti et al. 2017, PMID 28843015)
(Huh, 2021 #2538) PPMI,
↑ (~20%)
Ask Comp Bio
Brain
CSF (Xicoy, 2019 #2540)
2nd, Publication
available in sPD
(Xicoy, 2019 #2540)
2nd, Publication
available in sPD
(Xicoy, 2019 #2540)
2nd, Publication
available in sPD
PD onlyPD+ heterozHetero onlyGD onlyPD+GD
FibroblastGlcSph증거없네?

Uncertain Spans

locationtranscriptionuncertainty
Lewy pathology continuation paragrapho parkinsonism, LRRK2 has been found...The paragraph begins mid-sentence with o parkinsonism,; the leading words are clipped at the top of the section.
Positive vs Negative / a-syn / in vivo row12month homoz hippocampus에서만 올라가고, 12month homoz brain stem, 12month hetero, 12 week homo에선 안 올라갔음.Punctuation/spacing in mixed Korean-English text is preserved as visible source.
Postmortem matrix(Choi et al. 2011, PMID),The PMID number is not visible after PMID; the trailing comma is preserved.
Postmortem matrixcolumn-row alignment for the lower (Brain / CSF) duplicated rowsThe matrix has two Brain and two CSF rows; the lower pair appears to be a separate sub-section, but the leftmost label cell is partially clipped.