Fig. 2. Deficiency of neuronal HS leads to reduced neuroinflammation.

Slides:

Advertisements

Similar presentations

Comment on “ApoE-Directed Therapeutics Rapidly Clear β-Amyloid and Reverse Deficits in AD Mouse Models” by Karthikeyan Veeraraghavalu, Can Zhang, Sean.

Advertisements

Fig. 1. TP is highly expressed in myeloma.

Fig. 2. Increased Aβ plaque load in 16-month-old APP/PS1;C3 KO mice.

Cerebral Mast Cells Participate In Postoperative Cognitive Dysfunction by Promoting Astrocyte Activation Cell Physiol Biochem 2016;40: DOI: /

Aβ amyloid cortical and hippocampal pathology in McGill Thy1-APP transgenic (Tg) mice. A1: Absence of Aβ in non-transgenic (Non-Tg) littermate (ccx = cortex;

Fig. 4. Intramuscular injection of AAV9-Cas9/sgRNA-51 corrects dystrophin expression. Intramuscular injection of AAV9-Cas9/sgRNA-51 corrects dystrophin.

Fig. 6. C3 deficiency resulted in partial sparing of neuron loss in hippocampal CA3 in 16-month-old APP/PS1 mice. C3 deficiency resulted in partial sparing.

App‐CTFs accumulate in the neurites and synaptic compartments in Aph1abc cKO Cre+ brains App‐CTFs accumulate in the neurites and synaptic compartments.

Analysis of brain and spinal cord of treated Gaa−/− mice and controls

Volume 84, Issue 1, Pages (October 2014)

Fig. 1. Aberrant JNK pathway activation in mouse models of ALS and in spinal cord tissue from patients with sporadic ALS. Aberrant JNK pathway activation.

ApoE4 Accelerates Early Seeding of Amyloid Pathology

Comment on “ApoE-Directed Therapeutics Rapidly Clear β-Amyloid and Reverse Deficits in AD Mouse Models” by Ashleigh R. Price, Guilian Xu, Zoe B. Siemienski,

Fig. 4. Plaque-associated microglia and astrocytes and brain cytokines were altered in APP/PS1;C3 KO mice compared to APP/PS1 mice. Plaque-associated microglia.

Fig. 1. Neurobehavioral testing in YG8R mice transplanted with wild-type mouse HSPCs. Neurobehavioral testing in YG8R mice transplanted with wild-type.

Nec‐1 inhibits the phosphorylation and aggregation of tau

Fig. 5. Nutlin-3 treatment rescues the proliferation and differentiation of NPCs in vitro. Nutlin-3 treatment rescues the proliferation and differentiation.

BDNF expression in the cerebellum and brain stem region.

Volume 64, Issue 5, Pages (December 2009)

Fig. 3. Morphological changes associated with glial activation were reduced in 16-month-old APP/PS1;C3 KO mice. Morphological changes associated with glial.

Volume 17, Issue 5, Pages (May 2009)

Aβ Secretion and Plaque Formation Depend on Autophagy

Fig. 3 CSF1 is expressed in human melanoma.

Neuronal ATM level is reduced in mouse models of AD

Fig. 6 Transmissibility of adiposity from humanized mice to germ-free recipients. Transmissibility of adiposity from humanized mice to germ-free recipients.

Fig. 6 In utero injection of inflammatory cytokines or adoptive transfer of activated T cells leads to pregnancy loss. In utero injection of inflammatory.

Fig. 2. Spontaneous inflammasome activation by pyrin S242R.

Fig. 1. Generation of the ΔEx50 mouse model.

Filipin staining of marginal gyrus of cerebral cortex in NPC cats

Fig. 3. Features of PH in KRasLA2 transgenic mice.

Fig. 2. The N terminus of moZP2 decoys sperm in vitro and prevents mouse fertilization. The N terminus of moZP2 decoys sperm in vitro and prevents mouse.

Fig. 2 Propagation and misfolding of tau are enhanced with age.

Genetic EGFR ablation in K-RAS–mutated lung AC reduces tumor growth

Fig. 5. Anti-inflammatory effects of silibinin on KA treatment in the hippocampus. (A) Representative coronal sections of the hippocampal CA1 region following.

Fig. 5. Col IV–Ac2-26 NPs decrease lesion area, necrotic area, and oxidative stress in brachiocephalic arterial plaques. Col IV–Ac2-26 NPs decrease lesion.

Fig. 1. Potent and selective down-regulation of KRAS mRNA and protein by AZD4785 in vitro and in vivo. Potent and selective down-regulation of KRAS mRNA.

Fig. 1. DEL-1 is expressed by human and mouse osteoclasts.

The microchip-based drug delivery device and overview of study design

Fig. 3. Morphological changes associated with glial activation were reduced in 16-month-old APP/PS1;C3 KO mice. Morphological changes associated with glial.

TOMA does not affect NFTs in posterior hypothalamus or cortex.

Fig. 6. C3 deficiency resulted in partial sparing of neuron loss in hippocampal CA3 in 16-month-old APP/PS1 mice. C3 deficiency resulted in partial sparing.

by Yu Miyazaki, Xiaofei Du, Shin-ichi Muramatsu, and Christopher M

Fig. 3 Imaging-guided S-HDL nanoimmunotherapy in rabbits and pigs: PET-based readouts. Imaging-guided S-HDL nanoimmunotherapy in rabbits and pigs: PET-based.

Fig. 2 IRF8 is expressed in CD68+ macrophages after SCI.

by Gonghua Huang, Yanyan Wang, Peter Vogel, and Hongbo Chi

Fig. 2 NDR2-deficient mice are more vulnerable to RNA viral infection.

Compensatory metabolic pathways during long-term selegiline treatment

Fig. 2. Overexpression of miR cluster in the developing heart results in increased cardiomyocyte proliferation and cardiomegaly. Overexpression.

Fig. 3 Mmp-2−/− mice are protected from obesity and leptin resistance.

Fig. 4. Plaque-associated microglia and astrocytes and brain cytokines were altered in APP/PS1;C3 KO mice compared to APP/PS1 mice. Plaque-associated microglia.

Microfluidic platform for cell phenotype and gene function analysis

Fig. 6 Antitumor effect on tumor growth and pulmonary metastasis of CSSD-9 in vivo. Antitumor effect on tumor growth and pulmonary metastasis of CSSD-9.

Fig. 4. HERV-K env expression and injury to lower motor neurons.

Fig. 3. HERV-K–induced neuronal toxicity in vivo.

Fig. 4. miR promotes cardiomyocyte proliferation through regulation of Hippo pathway kinases. miR promotes cardiomyocyte proliferation through.

Passive immunization with CT α-syn antibodies improved TH pathology and neuroinflammation in the striatum of α-syn tg mice. Passive immunization with CT.

Fig. 2 Increasing KLF17, CDH1, and LASS2 expression reduced malignant progression and promoted apoptosis of tumor cells. Increasing KLF17, CDH1, and LASS2.

Fig. 7 BEL immune response.

Fig. 2. Col IV–Ac2-26 NPs increase subendothelial collagen in Ldlr−/− mice with established atherosclerosis. Col IV–Ac2-26 NPs increase subendothelial.

Fig. 7. Altered morphology after ultrasound but unaltered numbers of microglia in SUS-treated mice. Altered morphology after ultrasound but unaltered numbers.

Fig. 3. Association between peak CTL019 expansion and response.

Fig. 1. APP/PS1;C3 KO mice show improved cognitive flexibility (reversal) compared to APP/PS1 mice at 16 months of age. APP/PS1;C3 KO mice show improved.

Fig. 3. Col IV–Ac2-26 NPs suppress lesional superoxide and increase lesional Il10 mRNA in Ldlr−/− mice with established atherosclerosis. Col IV–Ac2-26.

Fig. 5. SUS treatment reduces Aβ in a second cohort of AD mice.

Fig. 3. SUS treatment reduces different Aβ species.

Fig. 6 Pharmacologic alterations of β-AR signaling regulate cardiomyocyte abscission and endowment. Pharmacologic alterations of β-AR signaling regulate.

Fig. 3 Correction of Dmd exon 44 deletion in mice by intramuscular AAV9 delivery of gene editing components. Correction of Dmd exon 44 deletion in mice.

Fig. 2. SUS reduces Aβ plaques in an AD mouse model.

Densin knock-out mice have normal gross neuroanatomy and low body weight. Densin knock-out mice have normal gross neuroanatomy and low body weight. A,

Fig. 6. Connectivity and mobility maps for Lesotho.

Presentation transcript:

Fig. 2. Deficiency of neuronal HS leads to reduced neuroinflammation. Deficiency of neuronal HS leads to reduced neuroinflammation. (A to C) Brain sections from APP/PS1 and APP/PS1; nExt1CKO mice at 12 months of age were immunostained with GFAP antibody. Scale bar, 1 mm. (B) Representative images of GFAP staining in the cortex and hippocampal CA1 region. Scale bar, 100 μm. (C) Stained sections were scanned on the Aperio slide scanner and analyzed using the ImageScope software. The percentage of areas covered by GFAP staining in the cortex (n = 11 to 13 per group) and hippocampus (n = 7 to 10 per group) was quantified. (D to F) Brain sections from APP/PS1 and APP/PS1; nExt1CKO mice at 12 months of age were immunostained with Iba1 antibody. Scale bar, 1 mm. (E) Representative images of Iba1 staining in the cortex and hippocampal CA1 region. Scale bar, 100 μm. (F) The percentage of area covered by Iba1 staining was quantified (n = 4 per group). (G) Amount of GFAP in the cortex (n = 9 per group) and hippocampus (n = 8 to 9 per group) of APP/PS1 and APP/PS1; nExt1CKO mice examined by Western blot. (H) Amounts of TNF-α, IL-1β, and IL-6 in the cortex of APP/PS1 and APP/PS1; nExt1CKO mice (n = 6 to 8 per group) evaluated by real-time PCR. Data represent means ± SEM. *P < 0.05; **P < 0.01. Statistical analysis was performed using Student’s t test. Chia-Chen Liu et al., Sci Transl Med 2016;8:332ra44 Copyright © 2016, American Association for the Advancement of Science