myeloid cells 2  (R&D Systems)

Journal: Alzheimer's & Dementia

Article Title: Sex and life experience shape locus coeruleus pretangle tau pathology

doi: 10.1002/alz.71285

Figure Lengend Snippet: Reduced tyrosine hydroxylase (TH) expression in the hippocampus of htauE14 rats and increased Brain‐Derived Neurotropic Factor (BDNF) expression following early enrichment. (A) Relative optical density (ROD) of TH expression across different groups. N = 4F/4M (cGFP), 6F/4M (cE14), 4F/2M (eSTR.E14), 3F/3M (eER.E14), 5F/3M (lSTR.E14), and 5F/1M (lER.E14). (B) ROD of BDNF expression, showing increased levels with early enrichment. N = 5F/5M (cGFP), 6F/6M (cE14), 6F/2M (eSTR.E14), 4F/4M (eER.E14), 6F/4M (lSTR.E14), and 6F/2M (lER.E14). (C) ROD of glucocorticoid receptor (GR) expression across groups. N = 5F/5M (cGFP), 6F/6M (cE14), 6F/2M (eSTR.E14), 4F/4M (eER.E14), 6F/4M (lSTR.E14), and 6F/2M (lER.E14). (D) ROD of Triggering Receptor Expressed on Myeloid cells 2 (TREM2) expression across groups. N = 5F/5M (cGFP), 6F/6M (cE14), 6F/2M (eSTR.E14), 4F/3M (eER.E14), 6F/4M (lSTR.E14), and 5F/2M (lER.E14). (E) ROD of tumor necrosis factor α (TNFα) expression across groups. N = 4F/5M (cGFP), 6F/5M (cE14), 5F/2M (eSTR.E14), 3F/4M (eER.E14), 6F/3M (lSTR.E14), and 5F/2M (lER.E14). * p < 0.05; ** p < 0.01.

Article Snippet: Membranes were stained with Ponceau S, blocked, and incubated with primary antibodies against brain‐derived neurotrophic factor (BDNF) (1:2000; Abcam, ab108319), glucocorticoid receptor (GR; 1:2000; Thermo Fisher Scientific, MA1‐510), Triggering Receptor Expressed on Myeloid Cells 2 (TREM2; 1:5000; R&D Systems; AF1729), TH (1:5000; Millipore Sigma, MAB318), tumor necrosis factor α (TNFα; 1:2000; Abcam, ab6671), DBH (1:2000; EMD Millipore, MAB508), s262 ptau (1:2000; Abcam, ab92627), T22 (1:2000; Millipore Sigma, ABN454) and Tau5 (1:3000, Millipore, 577801) followed by HRP‐conjugated secondary antibodies.

Techniques: Expressing, Derivative Assay

Journal: bioRxiv

Article Title: Therapeutic Targeting of Microglial Hexokinase-2 Recalibrates Inflammasome Activation and Improves Functional Recovery After Traumatic Brain Injury

doi: 10.64898/2026.03.01.708896

Figure Lengend Snippet: (A) Live-cell imaging–based efferocytosis assay using BV2 microglia incubated with fluorescently labeled apoptotic SH-SY5Y cells and 200 μM of LND for 48 hrs. (B) Quantification of BV2 cell confluency demonstrates reduced proliferation following LND treatment. ( n =4 per group, *p < 0.05, Multiple unpaired t-test followed by Two-stage linear step-up procedure of Benjamini, Krieger and Yekutieli) (C) LND treatment does not alter the efficiency or kinetics of apoptotic cell clearance. (D–F) qPCR analysis of a set of microglial activation–associated genes (polarization: HK2, Trem2, Tyrobp, and LPL) in the cortex and hippocampus of male mice following CCI and LND treatment. LND selectively reduces gene induction in the hippocampus. ( n = 7-8 per group, *p < 0.05, **p < 0.01, and ***p < 0.001, Ordinary one-way ANOVA with post hoc Tukey’s multiple comparisons) (G–I) Expression of inflammasome-related genes (Nlrp3, Asc, Casp1, Il1b and Tlr2) is robustly induced after CCI and significantly attenuated by LND in the hippocampus but not cortex. ( n = 7-8 per group, *p < 0.05, **p < 0.01, and ***p < 0.001, Ordinary one-way ANOVA with post hoc Tukey’s multiple comparisons)

Article Snippet: After one hour of blocking in 5% BSA (in PBS 1X), primary antibodies were applied overnight in blocking buffer at 4 °C: HK2 (1:1000, Abcam ab209847), HK1 (1:1000, Santa Cruz sc-46695), Trem2 (1:1000, R&D Systems AF1729), ASC (1:1000, Cell Signaling 67824S), and Beta Actin (Santa Cruz sc-130065).

Techniques: Live Cell Imaging, Incubation, Labeling, Activation Assay, Expressing

Journal: bioRxiv

Article Title: Therapeutic Targeting of Microglial Hexokinase-2 Recalibrates Inflammasome Activation and Improves Functional Recovery After Traumatic Brain Injury

doi: 10.64898/2026.03.01.708896

Figure Lengend Snippet: (A) Schematic of the experimental design using tamoxifen-inducible HK2 fl/wt mice, including recombination, CCI, and downstream analyses. (B–C) Representative images and quantification showing ∼50% reduction of HK2 immunoreactivity within IBA1⁺ microglia in the contralateral cortex following tamoxifen treatment. ( n = 7-11 per group, ****p < 0.0001, unpaired T test) (D) qPCR validation of reduced HK2 transcript levels in contralateral cortical tissue. ( n = 8 per group, *p < 0.05, unpaired T test) (E) Rotarod performance demonstrating improved motor coordination and endurance in HK2 heterozygous mice after CCI. ( n = 7-8 per group, ****p < 0.0001, Ordinary one-way ANOVA with post hoc Tukey’s multiple comparisons) (F) qPCR analysis showing reduced expression of HK1 and microglial activation markers (Trem2, Tyrobp, Cd68) in cortex following partial HK2 deletion. ( n = 7-8 per group, *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001, Ordinary one-way ANOVA with post hoc Tukey’s multiple comparisons)

Article Snippet: After one hour of blocking in 5% BSA (in PBS 1X), primary antibodies were applied overnight in blocking buffer at 4 °C: HK2 (1:1000, Abcam ab209847), HK1 (1:1000, Santa Cruz sc-46695), Trem2 (1:1000, R&D Systems AF1729), ASC (1:1000, Cell Signaling 67824S), and Beta Actin (Santa Cruz sc-130065).

Techniques: Biomarker Discovery, Expressing, Activation Assay