Amyloid β 42 protein inhib 
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  • ||||||||||  Alzheimer (In-Person) -  Jul 6, 2023 - Abstract #AAIC2023AAIC_1817;    
    These findings provide a novel conceptual framework for investigations of A? toxicity in the context of ?-secretase-dependent homeostatic signaling and raise the possibility that A?42-mediated inactivation of these enzymes contributes to AD development.
  • ||||||||||  Journal:  Imine-Linked Covalent Organic Framework Modulates Oxidative Stress in Alzheimer's Disease. (Pubmed Central) -  Jan 19, 2023   
    In vivo experiments indicated that SC@COF-T5 with a high blood-brain barrier (BBB) penetration efficiency was effective to reduce Aβ deposition, expression of pro-inflammatory cytokines, ROS levels, and neurologic damage in AD model mice, consequently rescuing memory deficits of AD mice. This work not only confirms the feasibility and merits of the therapeutic strategy regarding multiple targets for treatment of early AD pathogenesis but also opens up a novel direction for imine-linked COFs in biomedical applications.
  • ||||||||||  A NOVEL THERAPEUTIC APPROACH FOR ALZHEIMER (EXHIBITION) -  Dec 23, 2022 - Abstract #ADPD2023ADPD_1400;    
    secretase complex with APP. With this work, we expect to contribute to unveiling BRI2 as a neuronal differentiation modulator, which will be valuable to propose an innovative pro -neurogenic therapy for neurological conditions characterized by neuronal loss and a trophy, such as AD.
  • ||||||||||  Journal:  Intracellular Aβ42 Aggregation Leads to Cellular Thermogenesis. (Pubmed Central) -  Jun 11, 2022   
    We show that aggregation and heat retention by Aβ peptides are favored under intracellular-mimicking ionic conditions, which could potentially promote thermogenesis. The latter will, in turn, trigger further nucleation events that accelerate disease progression.
  • ||||||||||  PEDF-derived peptide inhibits Amyloid-β internalization and ameliorates retinal toxicity (F0450) -  Apr 29, 2022 - Abstract #ARVO2022ARVO_4386;    
    These observations provide evidence on the importance of extracellular versus intracellular Aβ42 in the retina and suggest that the mechanism of toxicity of fibrils possibly involves secondary release of oligomers. Such insights may promote the mechanistic understanding of the retinal pathogenicity of Aβ.
  • ||||||||||  Journal:  Activity-differential search for amyloid-β aggregation inhibitors using LC-MS combined with principal component analysis. (Pubmed Central) -  Mar 24, 2022   
    From 12 candidate compounds identified from the analysis, glucuronized and glucosidized quercetin, as well as 6 flavonoids (datiscetin, kaempferol, morin, robinetin, quercetin, and myricitrin), including catechol or flatness moiety suppressed Aβ42 aggregation, whereas curcumol, a sesquiterpene, did not. In conclusion, this study offers a new activity-differential methodology to identify bioactive natural products in crude drugs that inhibit Aβ42 aggregation and that could be applied to future AD therapies.
  • ||||||||||  Journal:  Amyloid-β peptide 37, 38 and 40 individually and cooperatively inhibit amyloid-β 42 aggregation. (Pubmed Central) -  Mar 23, 2022   
    Finally, we show that the aggregation of Aβ is more significantly impeded by a combination of Aβ, Aβ, and Aβ than by any of these alloforms independently. These results demonstrate that the aggregation of any given Aβ alloform is significantly perturbed by the presence of other alloforms, particularly in heterogeneous mixtures, such as is found in the extracellular fluid of the brain.
  • ||||||||||  Review, Journal:  Neoechinulins: Molecular, cellular, and functional attributes as promising therapeutics against cancer and other human diseases. (Pubmed Central) -  Mar 11, 2022   
    Alongside, it also inhibits cervical cancer cells by caspase-dependent apoptosis and via upregulation of apoptosis inducing genes like Bax, it suppresses LPS-induced inflammation in RAW264.7 macrophages and acts as an antidepressant. Whereas, another analogue, Neoechinulin B tends to interfere with the cellular mechanism thereby, inhibiting the entry of influenza A virus and it targets Liver X receptor (LXR) and decreases the infection rate of Hepatitis C. The present review describes the pharmaceutical properties of neoechinulins with notes on their molecular, cellular, and functional basis and their therapeutic properties.
  • ||||||||||  AN AΒ42 DOUBLE MUTANT INHIBITS AΒ42-INDUCED PLASMA AND MITOCHONDRIAL MEMBRANE DISRUPTION IN ARTIFICIAL MEMBRANES, ISOLATED ORGANS AND INTACT CELLS () -  Mar 9, 2022 - Abstract #ADPD2022ADPD_1312;    
    Whereas, another analogue, Neoechinulin B tends to interfere with the cellular mechanism thereby, inhibiting the entry of influenza A virus and it targets Liver X receptor (LXR) and decreases the infection rate of Hepatitis C. The present review describes the pharmaceutical properties of neoechinulins with notes on their molecular, cellular, and functional basis and their therapeutic properties. Overall, we provide a mechanistic explanation for the inhibitory activity of Aβ42DM against Aβ42-induced membrane permeability and cell toxicity and provide confirmatory evidence for its protective function in neuronal cells.
  • ||||||||||  Journal:  PEG-PEI/siROCK2 inhibits Aβ42-induced microglial inflammation via NLRP3/caspase 1 pathway. (Pubmed Central) -  Mar 8, 2022   
    Overall, we provide a mechanistic explanation for the inhibitory activity of Aβ42DM against Aβ42-induced membrane permeability and cell toxicity and provide confirmatory evidence for its protective function in neuronal cells. PPSR inhibits Aβ42-induced microglial inflammation via NLRP3/caspase 1 pathway.
  • ||||||||||  Journal:  Bcl-2-Homology-Only Proapoptotic Peptides Modulate β-Amyloid Aggregation and Toxicity. (Pubmed Central) -  Jan 27, 2022   
    In contrast, NOXA exhibited opposite effects, reducing Aβ42 fibril formation, affecting more pronounced apoptotic effects and mitochondrial disfunction, and enhancing membrane interactions of Aβ42. The effects of BID, PUMA, and NOXA upon the Aβ42 structure and toxicity may be linked to its biological properties and affect pathophysiological features of AD.
  • ||||||||||  Peptidomimetic-based vesicles inhibit amyloid-β fibrillation and attenuate cytotoxicity (Room: B313b - B314) -  Aug 13, 2021 - Abstract #ACSFall2021ACS_Fall_3929;    
    These vesicles completely rescue cells from the cytotoxicity that follows from Aβ42 misfolding. Biophysical studies, including confocal imaging, demonstrate the biocompatibility and selectivity of the approach towards this aberrant protein assembly in cellular milieu.
  • ||||||||||  CLR01 / UCLA
    Journal:  Different inhibitors of Aβ42-induced toxicity have distinct metal-ion dependency. (Pubmed Central) -  Jun 22, 2021   
    In agreement with these results, CLR01 inhibited β-sheet and fibril formation in Aβ42-Zn2+ complexes. Our data suggest that for development of efficient therapeutic agents, inhibitors of Aβ self-assembly and toxicity should be examined in the presence of relevant metal ions, and that molecular tweezers may be particularly attractive candidates for therapy development.
  • ||||||||||  Preclinical, Journal:  Ameliorative Properties of Boronic Compounds in In Vitro and In Vivo Models of Alzheimer's Disease. (Pubmed Central) -  Feb 24, 2021   
    Oral administration of 0.5 mg/kg dose of TBSA or an equivalent amount of methylcellulose vehicle to groups of six- and 12-month-old 5xFAD or wild-type mice over a two-month period prevented recognition- and spatial-memory deficits in the novel-object recognition and Morris-water-maze memory tasks, respectively, and reduced the number of pyknotic and degenerated cells, Aβ plaques, and GFAP and Iba-1 immunoreactivity in the hippocampus and cortex of these mice. These findings indicate that TBSA exerts neuroprotective properties by decreasing amyloid plaque burden and neuroinflammation, thereby preventing neuronal death and preserving memory function in the 5xFAD mice.
  • ||||||||||  Journal:  Estrogen protects neuroblastoma cell from amyloid-β 42 (Aβ42)-induced apoptosis via TXNIP/TRX axis and AMPK signaling. (Pubmed Central) -  Jan 26, 2021   
    Furthermore, the protective effects of estradiol against Aβ42-induced in vitro neurotoxicity on SH-SY5Y cells could be significantly reversed by AMPK inhibitor, Compound C, indicating that estradiol could improve Aβ42-induced AD via TXNIP/TRX and AMPK signaling. In summary, we demonstrated the cellular function of estradiol on Aβ42-induced in vitro neurotoxicity on SH-SY5Y cells and a novel mechanism of TXNIP/TRX axis involved in estradiol function via AMPK signaling.