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Article ; Online: Rescue of Alzheimer's disease phenotype in a mouse model by transplantation of wild-type hematopoietic stem and progenitor cells.

Mishra, Priyanka / Silva, Alexander / Sharma, Jay / Nguyen, Jacqueline / Pizzo, Donald P / Hinz, Denise / Sahoo, Debashis / Cherqui, Stephanie

Cell reports

2023 Volume 42, Issue 8, Page(s) 112956

Abstract: Alzheimer's disease (AD) is the most prevalent cause of dementia; microglia have been implicated in AD pathogenesis, but their role is still matter of debate. Our study showed that single systemic wild-type (WT) hematopoietic stem and progenitor cell ( ... ...

Abstract	Alzheimer's disease (AD) is the most prevalent cause of dementia; microglia have been implicated in AD pathogenesis, but their role is still matter of debate. Our study showed that single systemic wild-type (WT) hematopoietic stem and progenitor cell (HSPC) transplantation rescued the AD phenotype in 5xFAD mice and that transplantation may prevent microglia activation. Indeed, complete prevention of memory loss and neurocognitive impairment and decrease of β-amyloid plaques in the hippocampus and cortex were observed in the WT HSPC-transplanted 5xFAD mice compared with untreated 5xFAD mice and with mice transplanted with 5xFAD HSPCs. Neuroinflammation was also significantly reduced. Transcriptomic analysis revealed a significant decrease in gene expression related to "disease-associated microglia" in the cortex and "neurodegeneration-associated endothelial cells" in the hippocampus of the WT HSPC-transplanted 5xFAD mice compared with diseased controls. This work shows that HSPC transplant has the potential to prevent AD-associated complications and represents a promising therapeutic avenue for this disease.
MeSH term(s)	Mice ; Animals ; Alzheimer Disease/metabolism ; Endothelial Cells/metabolism ; Mice, Transgenic ; Amyloid beta-Peptides/metabolism ; Microglia/metabolism ; Phenotype ; Hematopoietic Stem Cell Transplantation ; Disease Models, Animal
Chemical Substances	Amyloid beta-Peptides
Language	English
Publishing date	2023-08-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2023.112956
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Article ; Online: Chronic villitis as a distinctive feature of placental injury in maternal SARS-CoV-2 infection.

Gabby, Lauryn C / Jones, Chelsea K / McIntyre, Brendan B / Manalo, Zoe / Meads, Morgan / Pizzo, Donald P / Diaz-Vigil, Jessica / Soncin, Francesca / Fisch, Kathleen M / Ramos, Gladys A / Jacobs, Marni B / Parast, Mana M

American journal of obstetrics and gynecology

2024

Abstract: Background: SARS-CoV-2 infection during pregnancy is associated with an increased risk for stillbirth, preeclampsia, and preterm birth. However, this does not seem to be caused by intrauterine fetal infection because vertical transmission is rarely ... ...

Abstract	Background: SARS-CoV-2 infection during pregnancy is associated with an increased risk for stillbirth, preeclampsia, and preterm birth. However, this does not seem to be caused by intrauterine fetal infection because vertical transmission is rarely reported. There is a paucity of data regarding the associated placental SARS-CoV-2 histopathology and their relationship with the timing and severity of infection. Objective: This study aimed to determine if maternal SARS-CoV-2 infection was associated with specific patterns of placental injury and if these findings differed by gestational age at time of infection or disease severity. Study design: A retrospective cohort study was performed at the University of California San Diego between March 2020 and February 2021. Placentas from pregnancies with a positive SARS-CoV-2 test were matched with 2 sets of controls; 1 set was time-matched by delivery date and sent to pathology for routine clinical indications, and the other was chosen from a cohort of placentas previously collected for research purposes without clinical indications for pathologic examination before the SARS-CoV-2 outbreak. Placental pathologic lesions were defined based on standard criteria and included maternal and fetal vascular malperfusion and acute and chronic inflammatory lesions. A bivariate analysis was performed using the independent Student t test and Pearson chi-square test. A logistic regression was used to control for relevant covariates. Regions of SARS-CoV-2-associated villitis were further investigated using protein-based digital spatial profiling assays on the GeoMx platform, validated by immunohistochemistry, and compared with cases of infectious villitis and villitis of unknown etiology. Differential expression analysis was performed to identify protein expression differences between these groups of villitis. Results: We included 272 SARS-CoV-2 positive cases, 272 time-matched controls, and 272 historic controls. The mean age of SARS-CoV-2 affected subjects was 30.1±5.5 years and the majority were Hispanic (53.7%) and parous (65.7%). SARS-CoV-2 placentas demonstrated a higher frequency of the 4 major patterns of placental injury (all P<.001) than the historic controls. SARS-CoV-2 placentas also showed a higher frequency of chronic villitis and severe chronic villitis (P=.03 for both) than the time-matched controls, which remained significant after controlling for gestational age at delivery (adjusted odds ratio, 1.52; 95% confidence interval, 1.01-2.28; adjusted odds ratio, 2.12; 95% confidence interval, 1.16-3.88, respectively). Digital spatial profiling revealed that programmed death-ligand 1 was increased in villitis-positive regions of the SARS-CoV-2 (logFC, 0.47; adjusted P value =.002) and villitis of unknown etiology (logFC, 0.58; adjusted P value =.003) cases, but it was conversely decreased in villitis-positive regions of the infectious villitis group (log FC, -1.40; adjusted P value <.001). Conclusion: Chronic villitis seems to be the most specific histopathologic finding associated with SARS-CoV-2 maternal infection. Chronic villitis involves damage to the vasculosyncytial membrane of the chorionic villi, which are involved in gas and nutrient exchange, suggesting potential mechanisms of placental (and perhaps neonatal) injury, even in the absence of vertical transmission. Surprisingly, changes in protein expression in SARS-CoV-2-associated villitis seem to be more similar to villitis of unknown etiology than to infectious villitis.
Language	English
Publishing date	2024-04-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	80016-8
ISSN	1097-6868 ; 0002-9378
ISSN (online)	1097-6868
ISSN	0002-9378
DOI	10.1016/j.ajog.2024.04.002
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Article ; Online: Selective tau seeding assays and isoform-specific antibodies define neuroanatomic distribution of progressive supranuclear palsy pathology arising in Alzheimer's disease.

Coughlin, David G / Goodwill, Vanessa S / Standke, Heidi G / Kim, Yongya / Coley, Nicolas / Pizzo, Donald P / Galasko, Douglas / Kraus, Allison / Hiniker, Annie

Acta neuropathologica

2022 Volume 144, Issue 4, Page(s) 789–792

MeSH term(s)	Alzheimer Disease/pathology ; Carbolines ; Humans ; Protein Isoforms ; Supranuclear Palsy, Progressive/pathology ; tau Proteins
Chemical Substances	Carbolines ; Protein Isoforms ; tau Proteins
Language	English
Publishing date	2022-08-18
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1079-0
ISSN	1432-0533 ; 0001-6322
ISSN (online)	1432-0533
ISSN	0001-6322
DOI	10.1007/s00401-022-02480-x
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Article ; Online: TDP-43 Pathology Exacerbates Cognitive Decline in Primary Age-Related Tauopathy.

Smirnov, Denis S / Salmon, David P / Galasko, Douglas / Edland, Steven D / Pizzo, Donald P / Goodwill, Vanessa / Hiniker, Annie

Annals of neurology

2022 Volume 92, Issue 3, Page(s) 425–438

Abstract: Objective: Primary age-related tauopathy (PART) refers to tau neurofibrillary tangles restricted largely to the medial temporal lobe in the absence of significant beta-amyloid plaques. PART has been associated with cognitive impairment, but ... ...

Abstract	Objective: Primary age-related tauopathy (PART) refers to tau neurofibrillary tangles restricted largely to the medial temporal lobe in the absence of significant beta-amyloid plaques. PART has been associated with cognitive impairment, but contributions from concomitant limbic age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) are underappreciated. Methods: We compare prevalence of LATE-NC and vascular copathologies in age- and Braak-matched patients with PART (n = 45, Braak stage I-IV, Thal phase 0-2) or early stage Alzheimer disease neuropathologic change (ADNC; n = 51, Braak I-IV, Thal 3-5), and examine their influence on clinical and cognitive decline. Results: Concomitant LATE-NC and vascular pathology were equally common, and cognition was equally impaired, in PART (Mini-Mental State Examination [MMSE] = 24.8 ± 6.9) and ADNC (MMSE = 24.2 ± 6.0). Patients with LATE-NC were more impaired than those without LATE-NC on the MMSE (by 5.8 points, 95% confidence interval [CI] = 3.0-8.6), Mattis Dementia Rating Scale (DRS; 17.5 points, 95% CI = 7.1-27.9), Clinical Dementia Rating, sum of boxes scale (CDR-sob; 5.2 points, 95% CI = 2.1-8.2), memory composite (0.8 standard deviations [SD], 95% CI = 0.1-1.6), and language composite (1.1 SD, 95% CI = 0.2-2.0), and more likely to receive a dementia diagnosis (odds ratio = 4.8, 95% CI = 1.5-18.0). Those with vascular pathology performed worse than those without on the DRS (by 10.2 points, 95% CI = 0.1-20.3) and executive composite (1.3 SD, 95% CI = 0.3-2.3). Cognition declined similarly in PART and ADNC over the 5 years preceding death; however, LATE-NC was associated with more rapid decline on the MMSE (β = 1.9, 95% CI = 0.9-3.0), DRS (β = 7.8, 95% CI = 3.4-12.7), CDR-sob (β = 1.9, 95% CI = 0.4-3.7), language composite (β = 0.5 SD, 95% CI = 0.1-0.8), and vascular pathology with more rapid decline on the DRS (β = 5.2, 95% CI = 0.6-10.2). Interpretation: LATE-NC, and to a lesser extent vascular copathology, exacerbate cognitive impairment and decline in PART and early stage ADNC. ANN NEUROL 2022;92:425-438.
MeSH term(s)	Alzheimer Disease/pathology ; Cognitive Dysfunction/pathology ; DNA-Binding Proteins ; Humans ; Neurofibrillary Tangles/pathology ; Plaque, Amyloid/pathology ; Tauopathies/pathology
Chemical Substances	DNA-Binding Proteins ; TARDBP protein, human
Language	English
Publishing date	2022-07-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	80362-5
ISSN	1531-8249 ; 0364-5134
ISSN (online)	1531-8249
ISSN	0364-5134
DOI	10.1002/ana.26438
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Zs.A 1370: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Identification of optimal conditions for human placental explant culture and extracellular vesicle release.

Tekkatte, Chandana / Lindsay, Scott A / Duggan, Erika / Castro-Martínez, Anelizze / Hakim, Abbas / Saldana, Isabella / Zhang, Yan / Zhou, Jun / Sebastian, Rachel / Liu, Yukun / Pontigon, Devin S / Meads, Morgan / Liu, Tzu Ning / Pizzo, Donald P / Nolan, John / Parast, Mana M / Laurent, Louise C

iScience

2023 Volume 26, Issue 10, Page(s) 108046

Abstract: Extracellular vesicles (EVs) can mediate intercellular communication, including signaling between the placenta and maternal tissues. Human placental explant culture is a ... ...

Abstract	Extracellular vesicles (EVs) can mediate intercellular communication, including signaling between the placenta and maternal tissues. Human placental explant culture is a versatile
Language	English
Publishing date	2023-09-26
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.108046
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Article ; Online: Serine-129 phosphorylation of α-synuclein is an activity-dependent trigger for physiologic protein-protein interactions and synaptic function.

Parra-Rivas, Leonardo A / Madhivanan, Kayalvizhi / Aulston, Brent D / Wang, Lina / Prakashchand, Dube Dheeraj / Boyer, Nicholas P / Saia-Cereda, Veronica M / Branes-Guerrero, Kristen / Pizzo, Donald P / Bagchi, Pritha / Sundar, V S / Tang, Yong / Das, Utpal / Scott, David A / Rangamani, Padmini / Ogawa, Yuki / Subhojit Roy

Neuron

2023 Volume 111, Issue 24, Page(s) 4006–4023.e10

Abstract: Phosphorylation of α-synuclein at the serine-129 site (α-syn Ser129P) is an established pathologic hallmark of synucleinopathies and a therapeutic target. In physiologic states, only a fraction of α-syn is phosphorylated at this site, and most studies ... ...

Abstract	Phosphorylation of α-synuclein at the serine-129 site (α-syn Ser129P) is an established pathologic hallmark of synucleinopathies and a therapeutic target. In physiologic states, only a fraction of α-syn is phosphorylated at this site, and most studies have focused on the pathologic roles of this post-translational modification. We found that unlike wild-type (WT) α-syn, which is widely expressed throughout the brain, the overall pattern of α-syn Ser129P is restricted, suggesting intrinsic regulation. Surprisingly, preventing Ser129P blocked activity-dependent synaptic attenuation by α-syn-thought to reflect its normal function. Exploring mechanisms, we found that neuronal activity augments Ser129P, which is a trigger for protein-protein interactions that are necessary for mediating α-syn function at the synapse. AlphaFold2-driven modeling and membrane-binding simulations suggest a scenario where Ser129P induces conformational changes that facilitate interactions with binding partners. Our experiments offer a new conceptual platform for investigating the role of Ser129 in synucleinopathies, with implications for drug development.
MeSH term(s)	Humans ; alpha-Synuclein/metabolism ; Phosphorylation ; Parkinson Disease/metabolism ; Synucleinopathies ; Serine/metabolism
Chemical Substances	alpha-Synuclein ; Serine (452VLY9402)
Language	English
Publishing date	2023-12-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	808167-0
ISSN	1097-4199 ; 0896-6273
ISSN (online)	1097-4199
ISSN	0896-6273
DOI	10.1016/j.neuron.2023.11.020
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Zs.A 2496: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Reply to: "Finding fibroblast growth factor 19 during cholestasis: Does x mark the spot?

Brandl, Katharina / Hartmann, Phillipp / Jih, Lily J / Pizzo, Donald P / Schnabl, Bernd

Journal of hepatology

2018 Volume 69, Issue 6, Page(s) 1400–1401

MeSH term(s)	Bile Acids and Salts ; Cholestasis ; Fibroblast Growth Factors ; Hepatitis, Alcoholic ; Humans
Chemical Substances	Bile Acids and Salts ; FGF19 protein, human ; Fibroblast Growth Factors (62031-54-3)
Language	English
Publishing date	2018-10-06
Publishing country	Netherlands
Document type	Letter ; Comment
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/j.jhep.2018.09.017
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Article ; Online: Neuronal Ndst1 depletion accelerates prion protein clearance and slows neurodegeneration in prion infection.

PLoS pathogens

2023 Volume 19, Issue 9, Page(s) e1011487

Abstract: Select prion diseases are characterized by widespread cerebral plaque-like deposits of amyloid fibrils enriched in heparan sulfate (HS), a abundant extracellular matrix component. HS facilitates fibril formation in vitro, yet how HS impacts fibrillar ... ...

Abstract	Select prion diseases are characterized by widespread cerebral plaque-like deposits of amyloid fibrils enriched in heparan sulfate (HS), a abundant extracellular matrix component. HS facilitates fibril formation in vitro, yet how HS impacts fibrillar plaque growth within the brain is unclear. Here we found that prion-bound HS chains are highly sulfated, and that the sulfation is essential for accelerating prion conversion in vitro. Using conditional knockout mice to deplete the HS sulfation enzyme, Ndst1 (N-deacetylase / N-sulfotransferase) from neurons or astrocytes, we investigated how reducing HS sulfation impacts survival and prion aggregate distribution during a prion infection. Neuronal Ndst1-depleted mice survived longer and showed fewer and smaller parenchymal plaques, shorter fibrils, and increased vascular amyloid, consistent with enhanced aggregate transit toward perivascular drainage channels. The prolonged survival was strain-dependent, affecting mice infected with extracellular, plaque-forming, but not membrane bound, prions. Live PET imaging revealed rapid clearance of recombinant prion protein monomers into the CSF of neuronal Ndst1- deficient mice, neuronal, further suggesting that HS sulfate groups hinder transit of extracellular prion protein monomers. Our results directly show how a host cofactor slows the spread of prion protein through the extracellular space and identify an enzyme to target to facilitate aggregate clearance.
MeSH term(s)	Animals ; Mice ; Heparitin Sulfate/metabolism ; Mice, Knockout ; Neurons/enzymology ; Prion Diseases/metabolism ; Prion Proteins/genetics ; Prions/metabolism ; Sulfotransferases/genetics ; Sulfotransferases/metabolism
Chemical Substances	Heparitin Sulfate (9050-30-0) ; Prion Proteins ; Prions ; heparitin sulfotransferase (EC 2.8.2.8) ; Sulfotransferases (EC 2.8.2.-)
Language	English
Publishing date	2023-09-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7374
ISSN (online)	1553-7374
ISSN	1553-7374
DOI	10.1371/journal.ppat.1011487
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Article ; Online: Diminished Neuronal ESCRT-0 Function Exacerbates AMPA Receptor Derangement and Accelerates Prion-Induced Neurodegeneration.

The Journal of neuroscience : the official journal of the Society for Neuroscience

2023 Volume 43, Issue 21, Page(s) 3970–3984

Abstract: Endolysosomal defects in neurons are central to the pathogenesis of prion and other neurodegenerative disorders. In prion disease, prion oligomers traffic through the multivesicular body (MVB) and are routed for degradation in lysosomes or for release in ...

Abstract	Endolysosomal defects in neurons are central to the pathogenesis of prion and other neurodegenerative disorders. In prion disease, prion oligomers traffic through the multivesicular body (MVB) and are routed for degradation in lysosomes or for release in exosomes, yet how prions impact proteostatic pathways is unclear. We found that prion-affected human and mouse brain showed a marked reduction in Hrs and STAM1 (ESCRT-0), which route ubiquitinated membrane proteins from early endosomes into MVBs. To determine how the reduction in ESCRT-0 impacts prion conversion and cellular toxicity
MeSH term(s)	Male ; Female ; Mice ; Humans ; Animals ; Prions/metabolism ; Prion Proteins/metabolism ; Receptors, AMPA/metabolism ; Neurons/metabolism ; Prion Diseases/metabolism ; Prion Diseases/pathology ; Neurodegenerative Diseases/metabolism ; Endosomal Sorting Complexes Required for Transport/metabolism
Chemical Substances	Prions ; Prion Proteins ; Receptors, AMPA ; Endosomal Sorting Complexes Required for Transport
Language	English
Publishing date	2023-04-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.1878-22.2023
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Article ; Online: Cancer-cell-secreted miR-122 suppresses O-GlcNAcylation to promote skeletal muscle proteolysis.

Yan, Wei / Cao, Minghui / Ruan, Xianhui / Jiang, Li / Lee, Sylvia / Lemanek, Adriana / Ghassemian, Majid / Pizzo, Donald P / Wan, Yuhao / Qiao, Yueqing / Chin, Andrew R / Duggan, Erika / Wang, Dong / Nolan, John P / Esko, Jeffrey D / Schenk, Simon / Wang, Shizhen Emily

Nature cell biology

2022 Volume 24, Issue 5, Page(s) 793–804

Abstract: A decline in skeletal muscle mass and low muscular strength are prognostic factors in advanced human cancers. Here we found that breast cancer suppressed O-linked N-acetylglucosamine (O-GlcNAc) protein modification in muscle through extracellular-vesicle- ...

Abstract	A decline in skeletal muscle mass and low muscular strength are prognostic factors in advanced human cancers. Here we found that breast cancer suppressed O-linked N-acetylglucosamine (O-GlcNAc) protein modification in muscle through extracellular-vesicle-encapsulated miR-122, which targets O-GlcNAc transferase (OGT). Mechanistically, O-GlcNAcylation of ryanodine receptor 1 (RYR1) competed with NEK10-mediated phosphorylation and increased K48-linked ubiquitination and proteasomal degradation; the miR-122-mediated decrease in OGT resulted in increased RYR1 abundance. We further found that muscular protein O-GlcNAcylation was regulated by hypoxia and lactate through HIF1A-dependent OGT promoter activation and was elevated after exercise. Suppressed O-GlcNAcylation in the setting of cancer, through increasing RYR1, led to higher cytosolic Ca
MeSH term(s)	Acetylglucosamine/metabolism ; Animals ; Humans ; Mice ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Muscle, Skeletal/metabolism ; N-Acetylglucosaminyltransferases/genetics ; Neoplasms/metabolism ; Protein Processing, Post-Translational ; Proteolysis ; Ryanodine Receptor Calcium Release Channel/metabolism
Chemical Substances	MIRN122 microRNA, human ; MicroRNAs ; Mirn122 microRNA, mouse ; Ryanodine Receptor Calcium Release Channel ; N-Acetylglucosaminyltransferases (EC 2.4.1.-) ; Acetylglucosamine (V956696549)
Language	English
Publishing date	2022-04-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1474722-4
ISSN	1476-4679 ; 1465-7392
ISSN (online)	1476-4679
ISSN	1465-7392
DOI	10.1038/s41556-022-00893-0
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