human anti beta ngf antibody  (R&D Systems)

Journal: bioRxiv

Article Title: Nanoliposomal Omega-3 Fatty Acids Promote Adult Hippocampal Neurogenesis through the BDNF/TrkB Pathway in C57BL/6 Mice

doi: 10.64898/2026.02.24.707750

Figure Lengend Snippet: Protein expression of molecules from the BDNF signaling pathway determined by Western Blot and representative membranes. (A)mBDNF. (B)TrkB. (C)proBDNF. (D)p75 for yogurt treated mice after 4 weeks. (E–F) Representative membranes showing signals for TrkB, mBDNF, pro-BDNF, and p75 in Control and fatty acids-treated mice. Data are expressed as mean ± SD, n =5−6/group. # 0.05 < p < 0.10; *p < 0.05; **p < 0.01; ***p < 0.001.

Article Snippet: Samples (50 μgr in 5× loading buffer) were then loaded into SDS-PAGE gels (12 or 15%) and transferred onto nitrocellulose membranes using the Mini-PROTEAN ® Tetra System (BIO-RAD) for 1 h. Membranes were incubated for 1 h with blocking solution (5% milk in TBST) and then probed overnight at 4°C with mouse anti-BDNF (1:2000; Icosagen; 327-100 clone 3C11), rabbit anti-p75 (1:700; Alomone Labs; ANT-007), rabbit anti-TrkB (1:700; Alomone Labs; ANT-019), and rabbit anti-proBDNF (1:2500; Genocopoeia) in TBST.

Techniques: Expressing, Western Blot, Control

Journal: Advanced Science

Article Title: Amyloid β Instigates Cardiac Neurotrophic Signaling Impairment, Driving Alzheimer's Associated Heart Disease

doi: 10.1002/advs.202511924

Figure Lengend Snippet: Alzheimer's disease pathology negatively impacts the neuro‐signaling pathway in the brain/heart axis of Tg2576 mice. (A,B): Representative immunoblots (A) and densitometric analysis (B) showing levels of NGF (n=5 vs. n=5, Student's t‐test P value 0.0023; Holm Sidak adjusted P value 0.0092), BDNF (n=5 vs. n=5, Student's t‐test P value 0.0250; Holm Sidak adjusted P value 0.0731), GAP‐43 (n=5 vs. n=4, Student's t‐test P value 0.0531; Holm Sidak adjusted P value 0.0531), and dβh (n=5 vs. n=5, Student's t‐test P value 0.0490; Holm Sidak adjusted P value 0.0956), in total heart tissue. In cerebral cortex lysates, NGF (n=5 vs. n=5, Student's t‐test P value 0.0034; Holm Sidak adjusted P value 0.0135), BDNF (n=3 vs. n=3, Student's t‐test P value 0.0069; Holm Sidak adjusted P value 0.0206), GAP‐43 (n=4 vs. n=4), and dβh (n=3 vs. n=4, Student's t‐test P value 0.0696; Holm Sidak adjusted P value 0.1343), from WT and Tg2576 mice. GAPDH levels were used as a loading control. (C–E): Digital images (C, scale bar 100 µm) and quantifications (D,E) showing cardiac adrenergic nerve fibers, labeled with anti‐tyrosine‐hydroxylase (TH, in green) (D), (n=4 vs. n=4, Student's t‐test P value 0.0060), and cardiac regenerating nerve endings, labeled with anti‐neuronal regeneration marker (GAP‐43, in red) (E), (n=4 vs. n=4, Student's t‐test P value 0.0170), in cardiac sections from WT and Tg2576 mice. Data are presented as a mean±SEM.

Article Snippet: Total lysates were used to evaluate the protein levels of NGF (Alomone labs, AN‐240; 1:1000), BDNF (Alomone labs, ANT‐010; 1:1000), GAP‐43 (Millipore, #AB552; 1:1000), Cleaved Caspase‐3‐ Asp175 (Cl‐Casp‐3, Cell Signaling, #94530; 1:500), dopamine β hydroxylase (DβH, Millipore, #AB1536; 1:1000), human Aβ [mouse monoclonal anti‐Aβ antibodies mixture composed of 4G8 epitope (residues Aβ18‐22, Covance, SIG‐39320; 1:1000) and 6E10 epitope (residues Aβ3‐8, Covance, SIG‐39220; 1:1000)], serum amyloid A3 (SAA3, Abcam, #ab231680; 1:500), TrkB [p Tyr816] (Novus Bio, #NBP1‐03499SS; 1:1000), TrkB (80E3) (Cell Signaling, #4603; 1:1000), phospho‐CREB (Ser133) (1B6) (Cell Signaling, #9196; 1:1000), CREB (Cell Signaling, #9197; 1:1000), p75NTR (Sigma Aldrich, 07‐476; 1:1000), fibronectin (Abcam, #ab2413; 1:1000), matrix metalloproteinases‐ 2 (MMP‐2, Cell Signaling, #35814; 1:1000), Laminin A/C (Santa Cruz Biotechnology, sc‐376248; 1:500), Actin (Millipore, MAB1501; 1:1000) and GAPDH (Santa Cruz Biotechnology, sc‐32233,6C5; 1: 2000), the three latter of which were used as loading controls.

Techniques: Western Blot, Control, Labeling, Marker

Journal: Advanced Science

Article Title: Amyloid β Instigates Cardiac Neurotrophic Signaling Impairment, Driving Alzheimer's Associated Heart Disease

doi: 10.1002/advs.202511924

Figure Lengend Snippet: Effects of human Aβ40 or Aβ42 oligomers on neurotrophic factors in neuronal cells (SH‐SY5Y) and human cardiomyocytes (AC16). (A,B): Representative immunoblots (A) and densitometric analysis (B) of multiple independent experiments to evaluate BDNF (n=9 vs. n=9, Student's t‐test P value 0.0008; Holm Sidak adjusted P value 0.0024), GAP‐43 (n=9 vs. n=9, Student's t‐test P value 0.0343; Holm Sidak adjusted P value 0.0674), and NGF (n=9 vs. n=9, Student's t‐test P value 0.5642), protein levels (B) in human neuroblastoma cells (SH‐SY5Y) stimulated with human Aβ40 oligomers for 16 h. (C,D): Representative immunoblots (C) and densitometric analysis (D) of multiple independent experiments to evaluate BDNF (n=9 vs. n=9, Student's t‐test P value 0.0093; Holm Sidak adjusted P value 0.0185), GAP‐43 (n=9 vs. n=9, Student's t‐test P value 0.0004; Holm Sidak adjusted P value 0.0012), and NGF (n=9 vs. n=9, Student's t‐test P value 0.6389), protein levels (D) in human neuroblastoma cells (SH‐SY5Y) stimulated with human Aβ42 oligomers for 16 h. GAPDH levels were used as a loading control. (E,F): Representative immunoblots (E) and densitometric quantitative analysis (F) showing protein levels of BDNF (upper panel) (n=7 vs. n=7, Student's t‐test P value 0.0025; Holm Sidak adjusted P value 0.005), and NGF (lower panel) (n=6 vs. n=6, Student's t‐test P value 0.6470) in total protein lysates from human cardiomyocytes (AC16) stimulated with human Aβ40 oligomers for 16 h. GAPDH levels were used as a loading control. (G,H) Representative immunoblots (G) and densitometric quantitative analysis (H) showing protein levels of BDNF (upper panel) (n=6 vs. n=6, Student's t‐test P value 0.7035), and NGF (lower panel) (n=6 vs. n=6, Student's t‐test P value 0.4618), in total protein lysates from human cardiomyocytes (AC16) stimulated with scrambled Aβ40 for 16 h. ACTIN and GAPDH levels were used as a loading control. Data are presented as a mean±SEM. (NT= Not Treated).

Article Snippet: Total lysates were used to evaluate the protein levels of NGF (Alomone labs, AN‐240; 1:1000), BDNF (Alomone labs, ANT‐010; 1:1000), GAP‐43 (Millipore, #AB552; 1:1000), Cleaved Caspase‐3‐ Asp175 (Cl‐Casp‐3, Cell Signaling, #94530; 1:500), dopamine β hydroxylase (DβH, Millipore, #AB1536; 1:1000), human Aβ [mouse monoclonal anti‐Aβ antibodies mixture composed of 4G8 epitope (residues Aβ18‐22, Covance, SIG‐39320; 1:1000) and 6E10 epitope (residues Aβ3‐8, Covance, SIG‐39220; 1:1000)], serum amyloid A3 (SAA3, Abcam, #ab231680; 1:500), TrkB [p Tyr816] (Novus Bio, #NBP1‐03499SS; 1:1000), TrkB (80E3) (Cell Signaling, #4603; 1:1000), phospho‐CREB (Ser133) (1B6) (Cell Signaling, #9196; 1:1000), CREB (Cell Signaling, #9197; 1:1000), p75NTR (Sigma Aldrich, 07‐476; 1:1000), fibronectin (Abcam, #ab2413; 1:1000), matrix metalloproteinases‐ 2 (MMP‐2, Cell Signaling, #35814; 1:1000), Laminin A/C (Santa Cruz Biotechnology, sc‐376248; 1:500), Actin (Millipore, MAB1501; 1:1000) and GAPDH (Santa Cruz Biotechnology, sc‐32233,6C5; 1: 2000), the three latter of which were used as loading controls.

Techniques: Western Blot, Control

Journal: Advanced Science

Article Title: Amyloid β Instigates Cardiac Neurotrophic Signaling Impairment, Driving Alzheimer's Associated Heart Disease

doi: 10.1002/advs.202511924

Figure Lengend Snippet: Myocardial neuro‐signaling impairment and Aβ deposits in human post‐mortem cardiac tissue of AD subjects. (A,B): Representative immunoblots (A) and densitometric analysis (B) showing reduced levels of BDNF (n=4 vs. n=7, Student's t‐test P value 0.0488; Holm Sidak adjusted P value 0.1605), GAP‐43 (n=4 vs. n=7, Student's t‐test P value 0.0428; Holm Sidak adjusted P value 0.1394), TH (n=4 vs. n=7, Student's t‐test P value 0.0516; Holm Sidak adjusted P value 0.1005), but not NGF (n=4 vs. n=7, Student's t‐test P value 0.3015), in total human LV lysates of patients with AD+CAA compared to healthy donors (CTRL). GAPDH levels were used as a loading control. (C,D): Representative digital images (C, scale bar 50 µm), and quantification (D) of the LV sections from CTRL and AD+CAA subjects stained with Aβ aggregates (in green) and cardiac Troponin I (cTnI, in red). (n=4 vs. n=7, Student's t‐test P value 0.0007). Data are presented as a mean±SEM.

Article Snippet: Total lysates were used to evaluate the protein levels of NGF (Alomone labs, AN‐240; 1:1000), BDNF (Alomone labs, ANT‐010; 1:1000), GAP‐43 (Millipore, #AB552; 1:1000), Cleaved Caspase‐3‐ Asp175 (Cl‐Casp‐3, Cell Signaling, #94530; 1:500), dopamine β hydroxylase (DβH, Millipore, #AB1536; 1:1000), human Aβ [mouse monoclonal anti‐Aβ antibodies mixture composed of 4G8 epitope (residues Aβ18‐22, Covance, SIG‐39320; 1:1000) and 6E10 epitope (residues Aβ3‐8, Covance, SIG‐39220; 1:1000)], serum amyloid A3 (SAA3, Abcam, #ab231680; 1:500), TrkB [p Tyr816] (Novus Bio, #NBP1‐03499SS; 1:1000), TrkB (80E3) (Cell Signaling, #4603; 1:1000), phospho‐CREB (Ser133) (1B6) (Cell Signaling, #9196; 1:1000), CREB (Cell Signaling, #9197; 1:1000), p75NTR (Sigma Aldrich, 07‐476; 1:1000), fibronectin (Abcam, #ab2413; 1:1000), matrix metalloproteinases‐ 2 (MMP‐2, Cell Signaling, #35814; 1:1000), Laminin A/C (Santa Cruz Biotechnology, sc‐376248; 1:500), Actin (Millipore, MAB1501; 1:1000) and GAPDH (Santa Cruz Biotechnology, sc‐32233,6C5; 1: 2000), the three latter of which were used as loading controls.

Techniques: Western Blot, Control, Staining