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BACKGROUND: Cost of illness studies are important tools to summarise the burden of disease for individuals, the healthcare system and society. The lack of standardised methods for reporting costs for cystic fibrosis (CF) makes it difficult to quantify the total socioeconomic burden. In this study, we aimed to comprehensively report the socioeconomic burden of CF in Canada. METHODS: The total cost of CF in Canada was calculated by triangulating information from three sources (Canadian CF Registry, customised Burden of Disease survey and publicly available information). A prevalence-based, bottom-up, human capital approach was applied, and costs were categorised into four perspectives (ie, healthcare system, individual/caregiver, variable (ie, medicines) and society) and three domains (ie, direct, indirect and intangible). All costs were converted into 2021 Canadian dollars (CAD) and adjusted for inflation. The cost of cystic fibrosis transmembrane conductance regulator (CFTR) modulator therapies was excluded. RESULTS: The total socioeconomic burden of CF in Canada in 2021 across the four perspectives was $C414 million. Direct costs accounted for two-thirds of the total costs, with medications comprising half of all direct costs. Out-of-pocket costs to individuals and caregivers represented 18.7% of all direct costs. Indirect costs representing absenteeism accounted for one-third of the total cost. CONCLUSION: This comprehensive cost of illness study for CF represents a community-oriented approach describing the socioeconomic burden of living with CF and serves as a benchmark for future studies.
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Costo de Enfermedad , Fibrosis Quística , Costos de la Atención en Salud , Humanos , Fibrosis Quística/economía , Fibrosis Quística/terapia , Fibrosis Quística/epidemiología , Canadá/epidemiología , Femenino , Masculino , Adulto , Costos de la Atención en Salud/estadística & datos numéricos , Adolescente , Adulto Joven , Niño , Gastos en Salud/estadística & datos numéricos , Preescolar , Cuidadores/economía , Factores Socioeconómicos , Lactante , Absentismo , Prevalencia , Persona de Mediana Edad , Sistema de RegistrosRESUMEN
Alzheimer's disease (AD) is the fifth leading cause of death among adults aged 65 and older, yet the onset and progression of the disease is poorly understood. What is known is that the presence of amyloid, particularly polymerized Aß42, defines when people are on the AD continuum. Interestingly, as AD progresses, less Aß42 is detectable in the plasma, a phenomenon thought to result from Aß becoming more aggregated in the brain and less Aß42 and Aß40 being transported from the brain to the plasma via the CSF. We propose that extracellular vesicles (EVs) play a role in this transport. EVs are found in bodily fluids such as blood, urine, and cerebrospinal fluid and carry diverse "cargos" of bioactive molecules (e.g., proteins, nucleic acids, lipids, metabolites) that dynamically reflect changes in the cells from which they are secreted. While Aß42 and Aß40 have been reported to be present in EVs, it is not known whether this interaction is specific for these peptides and thus whether amyloid-carrying EVs play a role in AD and/or serve as brain-specific biomarkers of the AD process. To determine if there is a specific interaction between Aß and EVs, we used isothermal titration calorimetry (ITC) and discovered that Aß42 and Aß40 bind to EVs in a manner that is sequence specific, saturable, and endothermic. In addition, Aß incubation with EVs overnight yielded larger amounts of bound Aß peptide that was fibrillar in structure. These findings point to a specific amyloid-EV interaction, a potential role for EVs in the transport of amyloid from the brain to the blood, and a role for this amyloid pool in the AD process.
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Enfermedad de Alzheimer , Vesículas Extracelulares , Adulto , Humanos , Péptidos , Proteínas Amiloidogénicas , PlasmaRESUMEN
Alzheimer's disease (AD), characterized by memory loss and cognitive decline, affects nearly 50 million people worldwide. Amyloid beta (Aß) plaques and intracellular neurofibrillary tangles (NFTs) of phosphorylated Tau protein (pTau) are key histopathological features of the disease in the brain, and recent advances have also identified AD histopathology in the retina. Thus, the retina represents a central nervous system (CNS) tissue highly amenable to non-invasive diagnostic imaging that shows promise as a biomarker for early AD. Given the devastating effects of AD on patients, their families, and society, new treatment modalities that can significantly alter the disease course are urgently needed. In this study, we have developed and characterized a novel human retinal organoid (RO) model derived from induced pluripotent stem cells (iPSCs) from patients with familial AD due to mutations in the amyloid precursor protein gene (APP). Using immunofluorescence and histological staining, we evaluated the cellular composition and AD histopathological features of AD-ROs compared to control ROs from healthy individuals. We found that AD-ROs largely resemble their healthy control counterparts in cellular composition but display increased levels of Aß and pTau. We also present proof of principle of an assay to quantify amyloid levels in whole ROs. This in vitro model of the human AD retina constitutes a new tool for drug screening, biomarker discovery, and pathophysiological studies.
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BACKGROUND: Cystic fibrosis (CF) contributes a significant economic burden on individuals, healthcare systems, and society. Understanding the economic impact of CF is crucial for planning resource allocation. METHODS: We conducted a scoping review of literature published between 1990 and 2022 that reported the cost of illness, and/or economic burden of CF. Costs were adjusted for inflation and reported as United States dollars. RESULTS: A total of 39 studies were included. Direct healthcare costs (e.g., medications, inpatient and outpatient care) were the most frequently reported. Most studies estimated the cost of CF using a prevalence-based (n = 18, 46.2 %), bottom-up approach (n = 23, 59 %). Direct non-healthcare costs and indirect costs were seldom included. The most frequently reported direct cost components were medications (n = 34, 87.2 %), inpatient care (n = 33, 84.6 %), and outpatient care (n = 31, 79.5 %). Twenty-eight percent (n = 11) of studies reported the burden of CF from all three perspectives (healthcare system (payer), individual, and society). Indirect costs of CF were reported in approximately 20 % of studies (n = 8). The reported total cost of CF varied widely, ranging from $451 to $160,000 per person per year (2022 US$). The total cost depended on the number of domains and perspectives included in each study. CONCLUSIONS: Most studies only reported costs to the healthcare system (i.e., hospitalizations and healthcare encounters) which likely underestimates the total costs of CF. The wide range of costs reported highlights the importance of standardizing perspectives, domains and costs when estimating the economic burden of CF.
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[This corrects the article on p. 336 in vol. 7, PMID: 27493838.].
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Microglia are central to pathogenesis in many neurological conditions. Drugs targeting colony-stimulating factor-1 receptor (CSF1R) to block microglial proliferation in preclinical disease models have shown mixed outcomes, thus the therapeutic potential of this approach remains unclear. Here, we show that CSF1R inhibitors given by multiple dosing paradigms in the Tg2541 tauopathy mouse model cause a sex-independent reduction in pathogenic tau and reversion of non-microglial gene expression patterns toward a normal wild type signature. Despite greater drug exposure in male mice, only female mice have functional rescue and extended survival. A dose-dependent upregulation of immediate early genes and neurotransmitter dysregulation are observed in the brains of male mice only, indicating that excitotoxicity may preclude functional benefits. Drug-resilient microglia in male mice exhibit morphological and gene expression patterns consistent with increased neuroinflammatory signaling, suggesting a mechanistic basis for sex-specific excitotoxicity. Complete microglial ablation is neither required nor desirable for neuroprotection and therapeutics targeting microglia must consider sex-dependent effects.
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Receptores de Factor Estimulante de Colonias de Granulocitos y Macrófagos , Tauopatías , Animales , Femenino , Masculino , Ratones , Encéfalo/metabolismo , Modelos Animales de Enfermedad , Microglía/metabolismo , Fenotipo , Receptores del Factor Estimulante de Colonias/genética , Receptores de Factor Estimulante de Colonias de Granulocitos y Macrófagos/antagonistas & inhibidores , Tauopatías/metabolismoRESUMEN
BACKGROUND: The ALLFTD (ARTFL-LEFFTDS Longitudinal Frontemporal Lobar Degeneration) study is an NIH-funded effort to prepare for clinical trials in sporadic (s-FTLD) and familial (f-FTLD) FTLD syndromes by characterizing cohorts, developing new clinical trial outcome measures, and evaluating disease progression. ALLFTD represents the merger and continuation of two prior studies: Advancing Research and Treatment of Frontotemporal Lobar Degeneration (ARTFL) and Longitudinal Evaluation of Familial Frontotemporal Dementia Subjects (LEFFTDS). METHODS: ALLFTD recruits participants with FTLD spectrum disorders (bvFTD, svPPA, nfvPPA, FTD-ALS, CBS or PSP), with strong family histories of FTLD, or known FTLD-associated genetic variants within the family. 26 sites in North America enroll participants for clinical and neuropsychological evaluations, MR Imaging, blood draws, and CSF collection in willing participants; participants are requested to return annually for follow-up evaluation. All participants are genotyped for dementia-associated mutations. Participants also enroll in the FTD Disorders Registry for follow-up surveys. A subset of participants undergo remote assessment via the ALLFTD app. Visits conducted under ARTFL and LEFFTDS are included in the ALLFTD dataset. RESULTS: ALLFTD has been successful in developing methods to conduct remote or hybrid visits and in actively evaluating participants. Since ALLFTD began in January 2020, 1034 participants (736 new; 298 previously enrolled in ARTFL or LEFFTDS) have been evaluated in the longitudinal arm; an additional 119 participants have been participated in a shortened, biofluid-focused visit. 349 have returned for follow-up visits. Including prior participants, the ALLFTD dataset contains 3871 visits from 2343 individuals. 1277 people have sporadic syndromes; 1045 were enrolled as familial. Among s-FTLD, bvFTD is the most common phenotype (32.8%) followed by PSP (15.9%). 61.4% of f-FTLD participants were clinically normal at first visit; bvFTD is the most common syndrome in symptomatic f-FTLD (40%). 477 are confirmed carriers of FTLD-associated genetic mutations. MRIs were obtained for 2594 visits; 3492 visits have associated blood biospecimens banked; 978 visits have associated CSF samples. CONCLUSIONS: The ALLFTD consortium is actively evaluating participants across North America to better characterize FTLD syndromes and support the planning and development of FTLD clinical trials. Longitudinal datasets including clinical, genetic, and imaging data are available by request.
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Demencia Frontotemporal , Humanos , Demencia Frontotemporal/genética , Degeneración Lobar Frontotemporal/genética , Estudios Longitudinales , Femenino , Masculino , Progresión de la Enfermedad , Persona de Mediana Edad , Anciano , Pruebas Neuropsicológicas/estadística & datos numéricosRESUMEN
In microscopy-based drug screens, fluorescent markers carry critical information on how compounds affect different biological processes. However, practical considerations, such as the labor and preparation formats needed to produce different image channels, hinders the use of certain fluorescent markers. Consequently, completed screens may lack biologically informative but experimentally impractical markers. Here, we present a deep learning method for overcoming these limitations. We accurately generated predicted fluorescent signals from other related markers and validated this new machine learning (ML) method on two biologically distinct datasets. We used the ML method to improve the selection of biologically active compounds for Alzheimer's disease (AD) from a completed high-content high-throughput screen (HCS) that had only contained the original markers. The ML method identified novel compounds that effectively blocked tau aggregation, which had been missed by traditional screening approaches unguided by ML. The method improved triaging efficiency of compound rankings over conventional rankings by raw image channels. We reproduced this ML pipeline on a biologically independent cancer-based dataset, demonstrating its generalizability. The approach is disease-agnostic and applicable across diverse fluorescence microscopy datasets.
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Previously, we found that amyloid-beta (Aß) competitively inhibits the kinesin motor protein KIF11 (Kinesin-5/Eg5), leading to defects in the microtubule network and in neurotransmitter and neurotrophin receptor localization and function. These biochemical and cell biological mechanisms for Aß-induced neuronal dysfunction may underlie learning and memory defects in Alzheimer's disease (AD). Here, we show that KIF11 overexpression rescues Aß-mediated decreases in dendritic spine density in cultured neurons and in long-term potentiation in hippocampal slices. Furthermore, Kif11 overexpression from a transgene prevented spatial learning deficits in the 5xFAD mouse model of AD. Finally, increased KIF11 expression in neuritic plaque-positive AD patients' brains was associated with better cognitive performance and higher expression of synaptic protein mRNAs. Taken together, these mechanistic biochemical, cell biological, electrophysiological, animal model, and human data identify KIF11 as a key target of Aß-mediated toxicity in AD, which damages synaptic structures and functions critical for learning and memory in AD.
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Myocardial infarction causes cardiomyocyte death and persistent inflammatory responses, which generate adverse pathological remodeling. Delivering therapeutic proteins from injectable materials in a controlled-release manner may present an effective biomedical approach for treating this disease. A thermoresponsive injectable gel composed of chitosan, conjugated with poly(N-isopropylacrylamide) and sulfonate groups, was developed for spatiotemporal protein delivery to protect cardiac function after myocardial infarction. The thermoresponsive gel delivered vascular endothelial growth factor (VEGF), interleukin-10 (IL-10), and platelet-derived growth factor (PDGF) in a sequential and sustained manner in vitro. An acute myocardial infarction mouse model was used to evaluate polymer biocompatibility and to determine therapeutic effects from the delivery system on cardiac function. Immunohistochemistry showed biocompatibility of the hydrogel, while the controlled delivery of the proteins reduced macrophage infiltration and increased vascularization. Echocardiography showed an improvement in ejection fraction and fractional shortening after injecting the thermal gel and proteins. A factorial design of experimental study was implemented to optimize the delivery system for the best combination and doses of proteins for further increasing stable vascularization and reducing inflammation using a subcutaneous injection mouse model. The results showed that VEGF, IL-10, and FGF-2 demonstrated significant contributions toward promoting long-term vascularization, while PDGF's effect was minimal.
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Infarto del Miocardio , Factor A de Crecimiento Endotelial Vascular , Animales , Hidrogeles/farmacología , Hidrogeles/uso terapéutico , Interleucina-10/uso terapéutico , Ratones , Infarto del Miocardio/tratamiento farmacológico , Infarto del Miocardio/patología , Factor A de Crecimiento Endotelial Vascular/metabolismo , Factor A de Crecimiento Endotelial Vascular/uso terapéuticoRESUMEN
BACKGROUND: The apolipoprotein E (APOE) ε4 allele confers the strongest risk for late-onset Alzheimer's disease (AD) besides age itself, but the mechanisms underlying this risk are debated. One hypothesis supported by evidence from multiple labs is that apoE4 binds to the amyloid-ß (Aß) peptide and catalyzes its polymerization into neurotoxic oligomers and fibrils. Inhibiting this early step in the amyloid cascade may thereby reduce or prevent neurodegeneration and AD. METHODS: Using a design of experiments (DOE) approach, we developed a high-throughput assay to identify inhibitors of apoE4-catalyzed polymerization of Aß into oligomers and fibrils. We used it to screen the NIH Clinical Collection of small molecule drugs tested previously in human clinical trials. We then evaluated the efficacy and cytotoxicity of the hit compounds in primary neuron models of apoE4-induced Aß and phosphorylated tau aggregation. Finally, we performed retrospective analyses of the National Alzheimer's Coordinating Center (NACC) clinical dataset, using Cox regression and Cox proportional hazards models to determine if the use of two FDA-approved hit compounds was associated with better cognitive scores (Mini-Mental State Exam), or improved AD clinical diagnosis, when compared with other medications of the same clinical indication. RESULTS: Our high-throughput screen identified eight blood-brain barrier (BBB)-permeable hit compounds that reduced apoE4-catalyzed Aß oligomer and fibril formation in a dose-dependent manner. Five hit compounds were non-toxic toward cultured neurons and also reduced apoE4-promoted Aß and tau neuropathology in a dose-dependent manner. Three of the five compounds were determined to be specific inhibitors of apoE4, whereas the other two compounds were Aß or tau aggregation inhibitors. When prescribed to AD patients for their normal clinical indications, two of the apoE4 inhibitors, imipramine and olanzapine, but not other (non-hit) antipsychotic or antidepressant medications, were associated with improvements in cognition and clinical diagnosis, especially among APOE4 carriers. CONCLUSIONS: The critical test of any proposed AD mechanism is whether it leads to effective treatments. Our high-throughput screen identified two promising FDA-approved drugs, imipramine and olanzapine, which have no structural, functional, or clinical similarities other than their shared ability to inhibit apoE4-catalyzed Aß polymerization, thus identifying this mechanism as an essential contribution of apoE4 to AD.
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Enfermedad de Alzheimer , Apolipoproteína E4 , Enfermedad de Alzheimer/metabolismo , Péptidos beta-Amiloides/metabolismo , Apolipoproteína E4/genética , Apolipoproteína E4/metabolismo , Catálisis , Cognición , Humanos , Imipramina/uso terapéutico , Olanzapina/uso terapéutico , Polimerizacion , Estudios RetrospectivosRESUMEN
Lithium-ion batteries (LIBs) are being used in locations and applications never imagined when they were first conceived. To enable this broad range of applications, it has become necessary for LIBs to be stable to an ever broader range of conditions, including temperature and energy. Unfortunately, while negative electrodes have received a great deal of focus in electrolyte development, stabilization of positive electrodes remains an elusive target. Here, we report a novel additive that shows the ability to protect positive electrodes against elevated temperatures and voltages. This additive can be used in small quantities, and its targeted behavior allows it to remain functional in complex electrolyte packages. This can prove an effective approach to targeting specific aspects of cell performance.
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Innate immune system activation and inflammation are associated with and may contribute to clinical outcomes in people with Down syndrome (DS), neurodegenerative diseases such as Alzheimer's disease (AD), and normal aging. In addition to serving as potential diagnostic biomarkers, innate immune system activation and inflammation may play a contributing or causal role in these conditions, leading to the hypothesis that effective therapies should seek to dampen their effects. However, recent intervention studies with the innate immune system activator granulocyte-macrophage colony-stimulating factor (GM-CSF) in animal models of DS, AD, and normal aging, and in an AD clinical trial suggest that activating the innate immune system and inflammation may instead be therapeutic. We consider evidence that DS, AD, and normal aging are accompanied by innate immune system activation and inflammation and discuss whether and when during the disease process it may be therapeutically beneficial to suppress or promote such activation.
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For common hydrogenation chemistries that occur at high temperatures (where H2 is adsorbed and activated at the same surface which the substrate must also adsorb for reaction), there is often little consensus on how the reactions (e.g., hydro(deoxy)genation) actually occur. We demonstrate here that an electrocatalytic palladium membrane reactor (ePMR) can be used to study hydrogenation reaction mechanisms at ambient temperatures, where the catalyst does not necessarily undergo structural reorganization. The ePMR uses electrolysis and a hydrogen-selective palladium membrane to deliver reactive hydrogen to a catalyst surface in an adjacent compartment for reaction with an organic substrate. This process forms the requisite metal-hydride surface for hydrogenation chemistry, but at ambient temperature and pressure, and without a H2 source. We demonstrate the utility of this analytical tool by studying the hydrogenation of benzaldehyde at palladium nanocubes with dimensions of 13-24 nm. This experimental design enabled us to resolve that the alcohol product forms at the facial sites, whereas the hydrodeoxygenation step occurs at edge sites. These observations enabled us to develop the first site-specific definition of how a carbonyl species undergoes hydro(deoxy)genation.
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BACKGROUND: Varicella zoster virus (VZV) vasculopathy is characterized by persistent arterial inflammation leading to stroke. Studies show that VZV induces amyloid formation that may aggravate vasculitis. Thus, we determined if VZV central nervous system infection produces amyloid. METHODS: Aß peptides, amylin, and amyloid were measured in cerebrospinal fluid (CSF) from 16 VZV vasculopathy subjects and 36 stroke controls. To determine if infection induced amyloid deposition, mock- and VZV-infected quiescent primary human perineurial cells (qHPNCs), present in vasculature, were analyzed for intracellular amyloidogenic transcripts/proteins and amyloid. Supernatants were assayed for amyloidogenic peptides and ability to induce amyloid formation. To determine amylin's function during infection, amylin was knocked down with small interfering RNA and viral complementary DNA (cDNA) was quantitated. RESULTS: Compared to controls, VZV vasculopathy CSF had increased amyloid that positively correlated with amylin and anti-VZV antibody levels; Aß40 was reduced and Aß42 unchanged. Intracellular amylin, Aß42, and amyloid were seen only in VZV-infected qHPNCs. VZV-infected supernatant formed amyloid fibrils following addition of amyloidogenic peptides. Amylin knockdown decreased viral cDNA. CONCLUSIONS: VZV infection increased levels of amyloidogenic peptides and amyloid in CSF and qHPNCs, indicating that VZV-induced amyloid deposition may contribute to persistent arterial inflammation in VZV vasculopathy. In addition, we identified a novel proviral function of amylin.
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Péptidos beta-Amiloides , Amiloide , Arteritis , Herpes Zóster , Polipéptido Amiloide de los Islotes Pancreáticos , Fragmentos de Péptidos , Amiloide/líquido cefalorraquídeo , Péptidos beta-Amiloides/líquido cefalorraquídeo , Arteritis/líquido cefalorraquídeo , Arteritis/diagnóstico , Arteritis/virología , ADN Complementario , ADN Viral , Herpes Zóster/líquido cefalorraquídeo , Herpes Zóster/diagnóstico , Herpesvirus Humano 3 , Humanos , Polipéptido Amiloide de los Islotes Pancreáticos/líquido cefalorraquídeo , Fragmentos de Péptidos/líquido cefalorraquídeo , Accidente CerebrovascularRESUMEN
BACKGROUND: Herpes zoster is linked to amyloid-associated diseases, including dementia, macular degeneration, and diabetes mellitus, in epidemiological studies. Thus, we examined whether varicella-zoster virus (VZV)-infected cells produce amyloid. METHODS: Production of intracellular amyloidogenic proteins (amylin, amyloid precursor protein [APP], and amyloid-ß [Aß]) and amyloid, as well as extracellular amylin, Aß, and amyloid, was compared between mock- and VZV-infected quiescent primary human spinal astrocytes (qHA-sps). The ability of supernatant from infected cells to induce amylin or Aß42 aggregation was quantitated. Finally, the amyloidogenic activity of viral peptides was examined. RESULTS: VZV-infected qHA-sps, but not mock-infected qHA-sps, contained intracellular amylin, APP, and/or Aß, and amyloid. No differences in extracellular amylin, Aß40, or Aß42 were detected, yet only supernatant from VZV-infected cells induced amylin aggregation and, to a lesser extent, Aß42 aggregation into amyloid fibrils. VZV glycoprotein B (gB) peptides assembled into fibrils and catalyzed amylin and Aß42 aggregation. CONCLUSIONS: VZV-infected qHA-sps produced intracellular amyloid and their extracellular environment promoted aggregation of cellular peptides into amyloid fibrils that may be due, in part, to VZV gB peptides. These findings suggest that together with host and other environmental factors, VZV infection may increase the toxic amyloid burden and contribute to amyloid-associated disease progression.
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Péptidos beta-Amiloides , Astrocitos , Polipéptido Amiloide de los Islotes Pancreáticos , Infección por el Virus de la Varicela-Zóster/metabolismo , Aciclovir/farmacología , Péptidos beta-Amiloides/química , Péptidos beta-Amiloides/metabolismo , Antivirales/farmacología , Astrocitos/efectos de los fármacos , Astrocitos/metabolismo , Astrocitos/virología , Células Cultivadas , Espacio Extracelular/metabolismo , Humanos , Espacio Intracelular/metabolismo , Polipéptido Amiloide de los Islotes Pancreáticos/química , Polipéptido Amiloide de los Islotes Pancreáticos/metabolismo , Proteínas del Envoltorio Viral/química , Proteínas del Envoltorio Viral/metabolismoRESUMEN
Crystal facets, vertices and edges govern the energy landscape of metal surfaces and thus the chemical interactions on the surface1,2. The facile absorption and desorption of hydrogen at a palladium surface provides a useful platform for defining how metal-solute interactions impact properties relevant to energy storage, catalysis and sensing3-5. Recent advances in in operando and in situ techniques have enabled the phase transitions of single palladium nanocrystals to be temporally and spatially tracked during hydrogen absorption6-11. We demonstrate herein that in situ X-ray diffraction can be used to track both hydrogen absorption and desorption in palladium nanocrystals. This ensemble measurement enabled us to delineate distinctive absorption and desorption mechanisms for nanocrystals containing exclusively (111) or (100) facets. We show that the rate of hydrogen absorption is higher for those nanocrystals containing a higher number of vertices, consistent with hydrogen absorption occurring quickly after ß-phase nucleation at lattice-strained vertices9,10. Tracking hydrogen desorption revealed initial desorption rates to be nearly tenfold faster for samples with (100) facets, presumably due to the faster recombination of surface hydrogen atoms. These results inspired us to make nanocrystals with a high number of vertices and (100) facets, which were found to accommodate fast hydrogen uptake and release.
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We demonstrate herein a CO2 reduction electrocatalyst regeneration strategy based on the manipulation of the Cu(0)/Cu2+ equilibrium with high concentrations of ethylenediaminetetraacetic acid (EDTA). This strategy enables the sustained performance of copper catalysts in distilled and tap water electrolytes for over 12 h. The deposition of common electrolyte impurities such as iron, nickel, and zinc is blocked because EDTA can effectively bind the metal ions and negatively shift the electrode potential of M/M n+. The Cu/Cu2+ redox couple is >600 mV more positive than the other metal ions and therefore participates in an equilibrium of dissolution and redeposition from and to the electrode in high concentrations of EDTA. These dynamic equilibria serve to further regenerate the surface copper catalyst to prevent the deactivation of catalytic sites. On the basis of this strategy, we show that >95% of initial hydrocarbon production activity can be maintained for 12 h in KHCO3 (99% purity) enriched distilled water and 6 h in KHCO3 (99% purity) enriched tap water.
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Electrochemically reducing CO2 using renewable energy is a contemporary global challenge that will only be met with electrocatalysts capable of efficiently converting CO2 into fuels and chemicals with high selectivity. Although many different metals and morphologies have been tested for CO2 electrocatalysis over the last several decades, relatively limited attention has been committed to the study of alloys for this application. Alloying is a promising method to tailor the geometric and electric environments of active sites. The parameter space for discovering new alloys for CO2 electrocatalysis is particularly large because of the myriad products that can be formed during CO2 reduction. In this Minireview, mixed-metal electrocatalyst compositions that have been evaluated for CO2 reduction are summarized. A distillation of the structure-property relationships gleaned from this survey are intended to help in the construction of guidelines for discovering new classes of alloys for the CO2 reduction reaction.