Results 111 to 120 of about 14,023 (271)

Bryostatin-1 vs. TPPB: Dose-Dependent APP Processing and PKC-α, -δ, and -ε Isoform Activation in SH-SY5Y Neuronal Cells [PDF]

, 2012
Activation of the α-secretase processing pathway of amyloid precursor protein (APP) is recognized as an important mechanism which diverts APP processing from production of beta-amyloid (Aβ) to non toxic sAPPα, decreasing Alzheimer’s disease (AD) plaque ...
J. S. Alexander, L. Schrott, P. Yi, T. P. Castor   +3 more
core   +1 more source

The causative role of amyloidosis in the cardiac complications of Alzheimer's disease: a comprehensive systematic review

The Journal of Physiology, Volume 604, Issue 4, Page 1646-1681, 15 February 2026.
Abstract figure legend Schematic illustration of the bidirectional causative link between cerebral amyloid‐beta (Aβ) angiopathy and cardiovascular disease in Alzheimer's disease (AD). Common cardiovascular risk factors like microvascular thrombosis, diabetes, atrial fibrillation, hypertension and atherosclerosis lead to cerebral hypoperfusion and ...
Samuel Parker, Andrew F. James, Svetlana Mastitskaya   +2 more
wiley   +1 more source

The resveratrol trimer miyabenol C inhibits β-secretase activity and β-amyloid generation.

PLoS ONE, 2015
Accumulation and deposition of amyloid-β peptide (Aβ) in the brain is a primary cause of the pathogenesis of Alzheimer's disease (AD). Aβ is generated from amyloid-β precursor protein (APP) through sequential cleavages first by β-secretase and then by γ ...
Jin Hu, Ting Lin, Yuehong Gao, Junyue Xu, Chao Jiang, Guanghui Wang, Guojun Bu, Huaxi Xu, Haifeng Chen, Yun-wu Zhang   +9 more
doaj   +1 more source

Familial Alzheimer’s disease mutations in amyloid protein precursor alter proteolysis by γ-secretase to increase amyloid β-peptides of ≥45 residues [PDF]

, 2021
Sujan Devkota, Todd D. Williams, Michael S. Wolfe   +2 more
openalex   +1 more source

Tetraspanin 6: a pivotal protein of the multiple vesicular body determining exosome release and lysosomal degradation of amyloid precursor protein fragments [PDF]

, 2017
BACKGROUND: The mechanisms behind Aβ-peptide accumulation in non-familial Alzheimer’s disease (AD) remain elusive. Proteins of the tetraspanin family modulate Aβ production by interacting to γ-secretase.
Annaert, W, Arranz, AM, Berditchevski, F, Colombelli, J, Corthout, N, De Strooper, B, Guix, FX, Horre, K, Kumar-Singh, S, Munck, S, Overduin, M, Radaelli, E, Rajesh, S, Saido, T, Saito, T, Salas, IH, Sannerud, R, Snellinx, A, Thathiah, A, Tosi, S   +19 more
core   +7 more sources

Alzheimer’s disease: pathogenesis, diagnostics, and therapeutics

International Journal of Nanomedicine, 2019
Sneham Tiwari, Venkata Atluri, Ajeet Kaushik, Adriana Yndart, Madhavan NairDepartment of Immunology and Nano-Medicine, Institute of NeuroImmune Pharmacology, Herbert Wertheim College of Medicine, Florida International University, Miami, FL 33199 ...
Tiwari S, Atluri V, Kaushik A, Yndart A, Nair M   +4 more
doaj  

Decrease in p3‐Alcβ37 and p3‐Alcβ40, products of Alcadein β generated by γ‐secretase cleavages, in aged monkeys and patients with Alzheimer's disease

Alzheimer’s & Dementia: Translational Research & Clinical Interventions, 2019
Introduction Neuronal p3‐Alcβ peptides are generated from the precursor protein Alcadein β (Alcβ) through cleavage by α‐ and γ‐secretases of the amyloid β (Aβ) protein precursor (APP).
Saori Hata, Chiori Omori, Ayano Kimura, Haruka Saito, Nobuyuki Kimura, Veer Gupta, Steve Pedrini, Eugene Hone, Pratishtha Chatterjee, Kevin Taddei, Kensaku Kasuga, Takeshi Ikeuchi, Masaaki Waragai, Masaki Nishimura, Anqi Hu, Tadashi Nakaya, Laurent Meijer, Masahiro Maeda, Tohru Yamamoto, Colin L. Masters, Chris C. Rowe, David Ames, Kazuo Yamamoto, Ralph N. Martins, Sam Gandy, Toshiharu Suzuki   +25 more
doaj   +1 more source

Identification and characterization of Aβ peptide interactors in Alzheimer’s disease by structural approaches

Frontiers in Aging Neuroscience, 2014
Currently, there are very limited pharmaceutical interventions for Alzheimer’s disease (AD) to alleviate the amyloid burden implicated in the pathophysiology of the disease.
Keith D Philibert, Robert A Marr, Eric M Norstrom, Marc J Glucksman   +3 more
doaj   +1 more source

Pharmacokinetics in Rat of P8, a Peptide Drug Candidate for the Treatment of Alzheimer’s Disease: Stability and Delivery to the Brain

Journal of Alzheimer's Disease Reports, 2018
Strategies to achieve a therapy for Alzheimer’s disease (AD) aimed at reducing the effects of amyloid-β (Aβ) have largely involved inhibiting or modifying the activities of the β- or γ -secretases or by the use of monoclonal antibodies (MAb).
Nazneen N. Dewji, Marc R. Azar, Leah R. Hanson, William H. Frey II, Bruce H. Morimoto, David Johnson   +5 more
doaj   +1 more source

Neuroprotective role of MMP-9 overexpression in the brain of Alzheimer's 5xFAD mice

Neurobiology of Disease, 2014
Accumulation of amyloid-β (Αβ) peptide is believed to play a central role in the pathogenesis of Alzheimer's disease (AD). Lowering Aβ levels in the brain may thus improve synaptic and cognitive deficits observed in AD patients.
Apostolia Fragkouli, Effie C. Tsilibary, Athina K. Tzinia   +2 more
doaj   +1 more source