총정리 GBA protein & activity (continued)

In CSF (20명) GlcCer: not measured ↑ LacCer, =GA2, ↑ GM3, ↓ GM2, ↓ GD3, ↓ GM1a, ↓ GD1A, ↓ GD1b, ↓ GT1b, ↓ Sum of these (61% of control)

In Serum (30명) =GlcCer, =LacCer, variable results in gangliosides (=Gb3, =Gb4, =GM3, =GM2, ↓ GM1a, ↓ GD1)

CitationRow labelNotes
(Boutin, 2016 #239)26↓ (trend) GlcCer in temporal cortex (only when normalized with GalCer isoform, might be due to ↑ GluCer as well as to ↓ GalCer)
(Nelson et al. 2018, PMID 29196214)GBA activityIn temporal cortex = in Braak stage II, III, ↓ in stage IV / ↓ (T369M, E326K one case each) / right edge: ↓↓
(Nelson et al. 2018, PMID 29196214)alpha-galactosidase AIn temporal cortex = in Braak stage II, III, ↓ in stage IV / = / right edge: =
(Nelson et al. 2018, PMID 29196214)a-syn= (vs PD only)
(Nelson et al. 2018, PMID 29196214)LAMP2In temporal cortex = in Braak stage II, III, ↓ in stage IV / No data
(Nelson et al. 2018, PMID 29196214)Cathepsin DIn temporal cortex: = in Braak stage II, III, ↓ in stage IV
(Nelson et al. 2018, PMID 29196214)Cathepsin BToo variable
(Gundner et al. 2019, PMID 30236861) postmortemGBA protein↓ trend (cortex, putamen, SN) / ↓ 39% in SN (differentiated) fig S3C
(Gundner et al. 2019, PMID 30236861) postmortemGBA activity↓ trend (cortex, putamen) / ↓ (23.8%, certainly not differentiated) fig S3
(Gundner et al. 2019, PMID 30236861) postmortemGlcSph ? 모두 안 통계유의 (10-30%, but 거의 overlap) (cortex, putamen, SN) / ↓ (30%, 안 통계유의, overlap될락말락, normal 군은 5이하이긴 하네.) FIG S3: 본문과 달리 GBA+PD/DLB만 모아놓음, median임. (Cortex에서만 통계적유의 & 1.6x, SN_fc=1.2. 안 통계유의, Putamen: fc 1.3, p=0.129) 본문fig3:GBA+ vs GBA- 환자들간에 차이도 없어 보임
(Chiasserini et al. 2015, PMID)GBA protein(할수 있었을 텐데) not done / right columns: 없음
(Chiasserini et al. 2015, PMID)GBA activity↓ than normal (by 23% in caudate) (by 12% in SN), no change in other regions
(Chiasserini et al. 2015, PMID)GBA mRNA↓ (SN)
Gegg 2015GBA protein↓ than normal; inset text includes Cbll 30% of control, Putamen: 72%, SN 60% / center column: ↓ than normal, Cbll 30% of control, SN 50%
Gegg 2015GBA activity
Gegg 2015GBA mRNANo change
(Murphy et al. 2014, PMID 24477431) postmortem brainGBA protein↓ (38%)(이유: cellular redistribution of a-syn and GBA) 즉 많아진 a-syn 때문에 ↑ GBA retention in ER / 왼쪽 결과는 anterior cingulate cortex에서의 감소결과임 / center/right: 없음
(Murphy et al. 2014, PMID 24477431) postmortem brainGBA activity↓ than normal (by 27%) / a-syn 없는 occipital cortex에서는 증가
(Murphy et al. 2014, PMID 24477431) postmortem brainGBA mRNA↓ trend only
(Murphy et al. 2014, PMID 24477431) postmortem brainaSyn
(Murphy et al. 2014, PMID 24477431) postmortem brainLysosomalLAMP1,2,3, Cathepsin ↑ A, ↑ D, =K, ↓ BECLIN1, =LC3II, Ceramide sphingomyelin
Rocha et al. 2015, PMID 25909088GBA protein안 봤음. / center/right: 없음
Rocha et al. 2015, PMID 25909088GBA activity↓ (and in aged normal control, too)
Rocha et al. 2015, PMID 25909088GBA mRNA안 봤음
Rocha et al. 2015, PMID 25909088GlcSph↑ 60' SN (trends in 70s & 80s SN), No change in putamen, ↑ hippocampus (nc in frontal cortex, cerebellum)
Gegg et al. 2012, MID 3034917) (post-mortem)GBA protein↓ (이유: ↓ gba binding to LIMP2) / ↓ (fig2a) differentiated / White bar: GBA+PD (cbll 30.4%, putamen 43.4%, SN 53.9%), Gray: GBA-PD / 없음 / in putamen & cerebellum 없음
Gegg et al. 2012, MID 3034917) (post-mortem)GBA activity↓ SN (33%) and cbll, putamen (by 19%), cerebellum (by 24%) / ↓ in all brain areas except frontal cx) SN (58% decrease), cerebellum (by 47%), frontal cortex (17%), amygdala (40%), and putamen (by 48%). (Average:42%)
Gegg et al. 2012, MID 3034917) (post-mortem)combined noteGba protein & activity 모두 normal control 대비 clearly differentiated
Gegg et al. 2012, MID 3034917) (post-mortem)GBA mRNANo change (저자: 아마도 d/t ↑ UPR) / center: No change
Gegg et al. 2012, MID 3034917) (post-mortem)Cathepsin DNo change / center: No change
Gegg et al. 2012, MID 3034917) (post-mortem)B-hexosaminidaseNo change / center: No change
Gegg et al. 2012, MID 3034917) (post-mortem)LC3IIMeasurement of LC3-II levels in the putamen did not differ significantly between the groups / center: LC3-II levels in the putamen did not differ significantly between the groups (N=4)
Gegg et al. 2012 / Gegg et al. 2015, PMID 096906Glucosylceramide No change in putamen & cerebellum ( / center: No change in putamen & cerebellum i. the residual function of the enzyme may be sufficient to prevent substrate accumulation, or ii. GlcCer accumulation is masked by shunting to these upstream gangliosides and other lipid species), iii. substrate accumulation in susceptible neurons might be masked by the more numerous glial cells (GBA와 Glucosylceramide 가 glial cell에도 존재하기는 하나, PD 에서 neuron이 죽으니, 여기서 이것들에 문제가 있다는 전제인 것 같음)
Gegg et al. 2012 / Gegg et al. 2015, PMID 096906GlucosylsphingosineNo change in cerebellum (↑ in putamen though, 하지만 GBA mutation 도 없이 증가되어봐야 무의미일 것) / center: No change in putamen & cerebellum
Gegg et al. 2012 / Gegg et al. 2015, PMID 096906GM2, GM3 gangliosidescenter: A trend of increase
oi et al. 2011, D), tmortem brainGBA proteinNormal과 비슷 / center: ↓ (조금) than normal, WB / right: 없음 and ↓↓ than normal (greatly diminished)
oi et al. 2011, D), tmortem brainGBA activityNormal과 비슷 / center: ↓ (35% of normal, N370S라고 적게 줄지 않았음.) / right edge: ↓↓ 4% of control, N370,L444다 심하게 감소
oi et al. 2011, D), tmortem brainGBA mRNA안 봤음.
zawa-Akanbi, 1 #2577) Postmortem (cingulate cortex)GlcCerGlcCer: = / center: GlcCer: =
zawa-Akanbi, #577) mortemGBA proteinNormal과 비슷 (저자도 이렇게 얘기하고 있음) Maybe this is not specifically from PD-related region? / center: ↓ 20% / right: ↓ 20% (저자가 말했음.) 근데 overlap B. Frontal cortex from 5개 (three N370S, L444P, RecNci) vs 정상뇌 107 / far right: 없음
zawa-Akanbi, #577) mortemGBA activityNormal과 비슷 (이게 다른 연구와 다른데, 여기선 사실 PD가 아니라 LBD임, 다른 연구에선 (아마 Chiasseri?)에선 LBD에선 GBA activity 감소가 경향만 있었던 것 같음. / center: ↓ 25% fig2보면 거의 clearly differentiated from normal control (우측 hetero only 와 같은 걸 보면, a-syn 이 GBA activity를 (bidirectioanally) 줄인다는 것은 안 맞는 것 같네. / right: ↓ 25%
zawa-Akanbi, #577) mortemGBA mRNA안 봤음.
zawa-Akanbi, #577) mortemLAMP1 / LAMP2
2020ATP13A2
2020Cathepsin D protein levelSpd 대비 약간 감소이나 정상인대비는 아니어서 해석 난망
2020 In vitroCathepsin D activityCathepsin D activity (Cathepsin D substrate solution (Enzo Life Sciences) → fluorescence
2020 In vitrocell sourcehuman neural crest stem cell derived dopaminergic neurons

Uncertain Spans

locationtranscriptionuncertainty
top continuationthe In CSF / In Serum lipid linesthe page begins mid-table; the preceding source label is in 20240722_182130.
Nelson rowsBraak stage II, III, ↓ in stage IVOCR sometimes confuses II / III / IV; preserved from visual/OCR agreement.
Gundner GlcSph notedense Korean statistical note (SN_fc=1.2, Putamen: fc 1.3, p=0.129, etc.)small line breaks and punctuation in the highlighted cell are uncertain.
Chiasserini source2015, PMIDThe PMID number is not visible in OCR/crop.
Gegg source linesGegg 2015, Gegg et al. 2012, MID 3034917, PMID 096906the leftmost source column is clipped and wrapped across multiple rows; PMID prefixes (MID vs PMID) read as written.
Murphy lysosomal rowCathepsin ↑ A, ↑ D, =K, ↓ BECLIN1the dense arrow/equality marks are small and span a narrow cell.
Lipid row paragraphi. ... ii. GlcCer accumulation is masked by shunting...the long italicised paragraph is small/tilted; transcribed from OCR/image evidence.
Clipped citationsoi et al. 2011, D), tmortem brain; zawa-Akanbi, 1 #2577); zawa-Akanbi, #577) mortem; 2020 In vitrothe leftmost citation column is clipped; only visible portions of names/dates are preserved.
bidirectioanallyreads as writtenlikely an authoring typo for bidirectionally.