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In real electric vehicles, the arrangement of liquid-cooled plates not only influences the thermal performance of the battery pack but also relates to the energy consumption of the BTMS and the compactness of the whole battery pack. In this study, design A, design B, design C, and design D, a total of four different arrangement designs of battery thermal management based on liquid-cooled plates with microchannels, are proposed for a 35 V battery pack composed of 12 LiFePO4 pouch battery cells connected in series, and the corresponding three-dimensional electrical-thermal-fluid model is established for numerical study. The cooling effects of the four designs are discussed and compared in terms of discharge rate, contact thermal resistance, and external short circuit. For design D, cold plates are placed in front of each battery cell. The results show that design D achieves the best cooling effect with the lowest power consumption compared to the other three designs under 0.5C, 1.0C, and 2.0C discharge rate. Its maximum temperature is about 30°C, and maximum temperature difference is under 5°C. The reduction in contact thermal resistance has different effects and magnitudes for different designs with different cold plate arrangements, but the overall effect is small. In the extreme condition of external short circuit, for design D, increasing the mass flow rate can reduce the maximum temperature of design D from 76.6°C by 27.5% to 55.5°C and the temperature difference from 35.0°C by 23.4% to 26.8°C. Selecting the proper coolant flow rate can keep the maximum temperature and temperature gradient on the battery pack of design D within tolerable level, and increasing the flow rate helps to enhance the cooling effect. For the other three designs, the maximum temperatures and temperature gradients exceeded 90°C and 40°C under the external short circuit condition, and increasing the flow rate has very little effect on the performance enhancement.

A new and efficient [3 + 2] cascade reaction has been developed for the synthesis of 3-aryl-3H-benzofuranone derivatives from aryl acetate via [3 + 2] annulation of 1,4-dihydroxy-2-naphthoic acid ester or 1,4-naphthoquinone.

Smartphones have become our daily necessities in the 21st century. Technology firms keep innovating new devices which provide customers variety of choices. Before buying a new smartphone, customers will usually search it online to watch some videos that evaluate each smartphone. To have a better idea of what how would customers consider before they purchase a smartphone, the authors have created a questionnaire with 45 respondents. The results show that Xiaomi benefits from its high-performance smartphones at a fair price. However, there are some drawbacks that Xiaomi does not satisfy people’s demand of vanity like apple did. Also, few places sell used smartphones as new phones and unauthorized smartphones which can damage brand reputation and lose customers. The results of this paper can help Xiaomi to have a better idea of how to improve its marketing strategies to satisfy more customers in India.

Variation in an animal's behavioral state is linked to fluctuations in brain activity and cognitive ability. In the neocortex, state-dependent circuit dynamics may reflect neuromodulatory influences such as that of acetylcholine (ACh). Although early literature suggested that ACh exerts broad, homogeneous control over cortical function, recent evidence indicates potential anatomical and functional segregation of cholinergic signaling. In addition, it is unclear whether states as defined by different behavioral markers reflect heterogeneous cholinergic and cortical network activity. Here, we perform simultaneous, dual-color mesoscopic imaging of both ACh and calcium across the neocortex of awake mice to investigate their relationships with behavioral variables. We find that higher arousal, categorized by different motor behaviors, is associated with spatiotemporally dynamic patterns of cholinergic modulation and enhanced large-scale network correlations. Overall, our findings demonstrate that ACh provides a highly dynamic and spatially heterogeneous signal that links fluctuations in behavior to functional reorganization of cortical networks.

Molecular imaging techniques have become important tools to characterize and measure biological processes at the cellular and molecular levels. Nowadays, molecular imaging techniques are widely used in preclinical and clinical studies to assess the molecular dynamics under physiological conditions and during pathological processes. This special issue on Brain Imaging (https://onlinelibrary.wiley.com/doi/toc/10.1111/[ISSN]1471-4159.brain-imaging) will highlight some of the recent advances in developing new tools and applying molecular imaging techniques to understand biomarker dynamics in health and diseases.

The endocannabinoid system (ECS) modulates synaptic function to regulate many aspects of neurophysiology. It adapts to environmental changes and is affected by disease. Thus, the ECS presents an important target for therapeutic development. Despite recent interest in cannabinoid-based treatments, few preclinical studies are conducted in human systems. Human induced pluripotent stem cells (hiPSCs) provide one possible solution to this issue. However, it is not known if these cells have a fully functional ECS. Here we show that hiPSC-derived neuron/astrocyte cultures exhibit a complete ECS. Using Ca

In the present study, a magnetically separable adsorbent, manganese ferrite (MnFe

Increasing extracellular levels of serotonin (5-HT) in the brain ameliorates symptoms of depression and anxiety-related disorders, e.g. social phobias and post-traumatic stress disorder. Recent evidence from preclinical and clinical studies established the potential of drugs inducing the release of 5-HT via the 5-HT-transporter. Nevertheless, current 5-HT releasing compounds under clinical investigation carry the risk for abuse and deleterious side effects. Here, we demonstrate that S-enantiomers of certain ring-substituted cathinones show preference for the release of 5-HT ex vivo and in vivo, and exert 5-HT-associated effects in preclinical behavioral models. Importantly, the lead cathinone compounds (i) do not induce substantial dopamine release and (ii) display reduced off-target activity at vesicular monoamine transporter-2 and 5-HT2B-receptors; indicative of low abuse-liability and low potential for adverse events. Taken together, our findings identify these agents as first-in class leads that may prove useful for the treatment of disorders where elevation of 5-HT has proven beneficial.

A fundamental challenge in fluorescence microscopy is the photon shot noise arising from the inevitable stochasticity of photon detection. Noise increases measurement uncertainty and limits imaging resolution, speed and sensitivity. To achieve high-sensitivity fluorescence imaging beyond the shot-noise limit, we present DeepCAD-RT, a self-supervised deep learning method for real-time noise suppression. Based on our previous framework DeepCAD, we reduced the number of network parameters by 94%, memory consumption by 27-fold and processing time by a factor of 20, allowing real-time processing on a two-photon microscope. A high imaging signal-to-noise ratio can be acquired with tenfold fewer photons than in standard imaging approaches. We demonstrate the utility of DeepCAD-RT in a series of photon-limited experiments, including in vivo calcium imaging of mice, zebrafish larva and fruit flies, recording of three-dimensional (3D) migration of neutrophils after acute brain injury and imaging of 3D dynamics of cortical ATP release. DeepCAD-RT will facilitate the morphological and functional interrogation of biological dynamics with a minimal photon budget.

This work investigated the fatigue crack propagation behavior of the 2195-T8 Al-Li alloy with precorroded holes. The microstructure, crack growth path, and the fracture surfaces of the samples with the precorroded holes have been examined with scanning electron microscopy (SEM), electron backscatter diffraction (EBSD), and computed tomography (CT). The characteristics of the crack growth have been analyzed via fracture mechanics by employing the finite element method (FEM). The results showed that the bulk of the fatigue cracks had been initiated from the corrosion pits and corroded discontinuously and precipitated further to become intergranular. Owing to the superposed stress concentration caused by the corrosion pits, the porous region at the bottom of the precorroded hole had affected the crack propagation performance. Crack growth rates were different in multiple positions owing to the difference of K I at crack fronts.

PurposeProsocial lending in online crowdfunding has flourished in recent years, and it has become a new way to fundraise for philanthropy. However, there is almost a 70% user attrition rate in crowdfunding. The purpose of this study is to understand what the lender’s lending experience and social connection influence lender retention of online prosocial lending from a self-determination perspective.Design/methodology/approachDrawing on self-determination theory (SDT), this research utilizes a quantifiable method for factors of the lender's lending experience and social connection. Additionally, the research constructs economic models to explore the impacts of these factors acting as the necessary conditions for basic psychological needs on lender retention, using a large-scale sample of over 380,000 lenders from Kiva.FindingsThe results indicate that, from the lender's lending experience aspect, the loan narratives with more profit language in the last lending and the failure of past participation are negatively related to lender retention. Regarding the lender's social connection aspect, their friends or small lending teams are positively related to lender retention, while whether they are invited and lending team size show negative influence. Furthermore, results indicate the moderating effects of the disclosure of lending motivation.Originality/valueThis research explores the mechanism of lender retention of online prosocial lending, providing a self-determination perspective about how previous experience influences long-term lending behavior. The study offers significant implications for the literature on online philanthropy, SDT and user retention of online platforms. At the same time, the study provides an understanding of the effects of different aspects of SDT.

The dynamic biaxial compression test for carbon-fiber-reinforced polymer (CFRP) laminates was carried out via synchronous electromagnetic loading in this study. During the experiments, four stress pulses transmitted along four incident bars, loading the square specimen simultaneously from four directions to keep the center of the specimen still. The dynamic mechanical behavior of CFRP was obtained employing the one-dimensional wave propagation theory, and the deformation and failure processes of the specimens were recorded by a high-speed camera. The effects of various biaxial stresses on the compressive strength were investigated in three biaxial and one uniaxial loading cases. For the CFRP laminates, the dynamic transverse compressive stress showed little effect on the longitudinal ultimate compressive strength. Numerical simulations were performed to understand the dynamic stress wave propagation. It showed that the employed loading device could guarantee good biaxial loading conditions until the ultimate failure of the specimens. This approach allows for the dynamic biaxial compression testing of various materials, which is of great significance in evaluating the dynamic impact performance of aeronautical composites.

Midbrain and striatal dopamine signals have been extremely well characterized over the past several decades, yet novel dopamine signals and functions in reward learning and motivation continue to emerge. A similar characterization of real-time sub-second dopamine signals in areas outside of the striatum has been limited. Recent advances in fluorescent sensor technology and fiber photometry permit measurement of dopamine binding correlates, which can divulge basic functions of dopamine signaling in non-striatal dopamine terminal regions, like the dorsal bed nucleus of the stria terminalis (dBNST). Here, we record GRABDAsignals in the dBNST during a Pavlovian lever autoshaping task. We observe greater Pavlovian cue-evoked dBNST GRABDAsignals in sign-tracking (ST) compared to goal-tracking/intermediate (GT/INT) rats and the magnitude of cue-evoked dBNST GRABDAsignals decrease immediately following reinforcer-specific satiety. When we deliver unexpected reward or omit expected reward, we find that dBNST dopamine signals encode bidirectional reward prediction errors in GT/INT rats, but only positive prediction errors in ST rats. Since sign- and goal-tracking approach strategies are associated with distinct drug relapse vulnerabilities, we examined the effects of experimenter-administered fentanyl on dBNST dopamine associative encoding. Systemic fentanyl injections do not disrupt dBNST cue discrimination but generally potentiate dBNST dopamine signals. These results reveal multiple dBNST dopamine correlates of learning and motivation that depend on the Pavlovian approach strategy employed.

The hypothalamic suprachiasmatic nucleus (SCN) is the master mammalian circadian clock. Its cell-autonomous timing mechanism, a transcriptional/translational feedback loop (TTFL), drives daily peaks of neuronal electrical activity, which in turn control circadian behavior. Intercellular signals, mediated by neuropeptides, synchronize and amplify TTFL and electrical rhythms across the circuit. SCN neurons are GABAergic, but the role of GABA in circuit-level timekeeping is unclear. How can a GABAergic circuit sustain circadian cycles of electrical activity, when such increased neuronal firing should become inhibitory to the network? To explore this paradox, we show that SCN slices expressing the GABA sensor iGABASnFR demonstrate a circadian oscillation of extracellular GABA ([GABA] e ) that, counterintuitively, runs in antiphase to neuronal activity, with a prolonged peak in circadian night and a pronounced trough in circadian day. Resolving this unexpected relationship, we found that [GABA] e is regulated by GABA transporters (GATs), with uptake peaking during circadian day, hence the daytime trough and nighttime peak. This uptake is mediated by the astrocytically expressed transporter GAT3 ( Slc6a11 ), expression of which is circadian-regulated, being elevated in daytime. Clearance of [GABA] e in circadian day facilitates neuronal firing and is necessary for circadian release of the neuropeptide vasoactive intestinal peptide, a critical regulator of TTFL and circuit-level rhythmicity. Finally, we show that genetic complementation of the astrocytic TTFL alone, in otherwise clockless SCN, is sufficient to drive [GABA] e rhythms and control network timekeeping. Thus, astrocytic clocks maintain the SCN circadian clockwork by temporally controlling GABAergic inhibition of SCN neurons.

PurposeThe numerous spoil grounds brought about by mega transportation infrastructure projects which can be influenced by the ecological environment. To achieve better management of spoil grounds, this paper aims to assess their comprehensive risk levels and categorize them into different categories based on ecological environmental risks.Design/methodology/approachBased on analysis of the environmental characteristics of spoil grounds, this paper first comprehensively identified the ecological environmental risk factors and developed a risk assessment index system to quantitatively describe the comprehensive risk levels. Second, this paper proposed a comprehensive model to determine the risk assessment and categorization of spoil ground group in mega projects integrating improved projection pursuit clustering (PPC) method and K-means clustering algorithm. Finally, a case study of a spoil ground group (includes 50 spoil grounds) in a mega infrastructure project in western China is presented to demonstrate and validate the proposed method.FindingsThe results show that our proposed comprehensive model can efficiently assess and categorize the spoil grounds in the group based on their comprehensive ecological environmental risk. In addition, during the process of risk assessment and categorization of spoil grounds, it is necessary to distinguish between sensitive factors and nonsensitive factors. The differences between different categories of spoil grounds can be recognized based on nonsensitive factors, and high-risk spoil grounds which need to be focused more on can be identified according to sensitive factors.Originality/valueThis paper develops a comprehensive model of risk assessment and categorization of a group of spoil grounds based on their ecological environmental risks, which can provide a reference for the management of spoil grounds in mega projects.

Adaptation to potential threat cues in feeding regulation is key for animal survival. Maladaptation in balancing internal energy needs and external threat cues may result in eating disorders. However, brain mechanisms underlying such maladaptation remain elusive. Here, we identified that the basal forebrain (BF) sends glutamatergic projections to glutamatergic neurons in the ventral tegmental area (VTA). Glutamatergic neurons in both the BF and the VTA displayed correlated responses to various external stressors. Notably,in vivomanipulation of BF terminals in the VTA revealed that the glutamatergic BF➔VTA circuit reduces appetite, increases locomotion, and elicits avoidance. In consistence, activation of VTA glutamatergic neurons reduced body weight, blunted food motivation, and caused hyperactivity with behavioral signs of anxiety, all hallmarks of typical anorexia phenotypes. Importantly, activation of BF glutamatergic terminals in the VTA reduced dopamine release in the nucleus accumbens (NAc). Collectively, our results point to overactivation of the glutamatergic BF➔VTA circuit as a potential cause of anorexia-like phenotypes involving reduced dopamine release.

Myocardial infarction (MI)-induced ventricular arrhythmia is the most common cause of death in patients with type 2 diabetes mellitus (T2DM). Patients with T2DM are two to four times more likely to die from MI than non-diabetic patients. Withdrawal of cardiac vagal activity is an important trigger for MI-induced ventricular arrhythmias in T2DM. Our recent study found that T2DM-elevated hydrogen peroxide (H2O2) levels in cardiac vagal postganglionic (CVP) neurons contribute to the withdrawal of cardiac vagal activity and ventricular arrhythmogenesis through inhibition of N-type Ca2+ channels (Cav2.2) in CVP neurons. The repressor element 1-silencing transcription factor (REST) is crucial to inhibit the expression of Cav2.2-α. In general, mature neuronal cells do not express the REST in the physiological condition. Here, we tested whether H2O2 induces REST expression in CVP neurons, which successively inhibits the expression of Cav2.2 in CVP neurons, causes cardiac vagal dysfunction, and triggers MI-evoked ventricular arrhythmias in T2DM rats. Our in vitro experiments demonstrated that protein expression of REST is high, whereas Cav2.2-α expression is low in undifferentiated NG108-15 cells. Differentiation of NG108-15 cells for twenty-one days significantly reduced REST expression and increased Cav2.2-α expression. Additionally, treatment with exogenous H2O2 (1 μM) in differentiated NG108-15 cells markedly increased REST expression and decreased Cav2.2-α expression. Similarly, a high level of REST protein and a low level of Cav2.2-α protein were confirmed in CVP neurons from T2DM rats than those from age-matched sham rats. In vivo transfection of REST shRNA (2 μl, 1×107 TU/ml) into the CVP neurons significantly decreased REST expression and increased Cav2.2-α expression in CVP neurons from T2DM rats. REST shRNA also improved cardiac vagal function, measured by heart rate variability, and reduced the cumulative duration of MI-evoked ventricular arrhythmias in conscious rats. These data suggested that H2O2-REST signaling pathway could be a key factor to mediate cardiac vagal dysfunction and affect the occurrence of ventricular arrhythmias in T2DM. This study was supported by the NIH-NHLBI (R01HL144146 to YLL). This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Peripheral artery disease (PAD) is primarily caused by occlusion of arteries that supply blood to the lower limbs and presents significantly pathological changes of calf muscles, include degenerating and regenerating fibers, reduction of the skeletal muscle area, connective tissue proliferation and fibrosis, fat accumulation, and abnormal mitochondria, all of which are predictors of muscle functional decline. Additionally, skeletal muscles also require the motor nerve innervation for the signal transmission through the neuromuscular junction (NMJ) to induce skeletal muscle contraction. To observe whether the NMJ is changed in the PAD patients, gastrocnemius muscles were collected from 2 health subjects and 6 PAD stage III/IV patients. The motor nerve terminals were labeled with anti-neurofilament 200 and anti-synaptophysin antibodies, the nicotinic acetylcholine receptors (nAChRs) were labeled with α-Bungarotoxin. Labeled NMJs were imaged using a laser scanning confocal microscope with Z-stack. The image was captured in 65 NMJs from health subjects and 140 NMJs from PAD patients, respectively. The total nAChR area and the number of discrete fragments of each nAChR cluster, the area per fragment, the percentage of fragmented nAChR clusters, the nerve innervation and the nerve terminal occupancy were calculated. The results were represented with mean ± standard error (SE). The nAChR area was 354.9 ± 12.7 and 209.4 ± 8.2, the average number of fragment/ nAChR cluster was 2.6 ± 0.2 and 3.1 ± 0.2, 6.2% and 19.3% of the nAChR clusters were fragmented, and the nerve terminal occupancy was 61.5 ± 1.4 % and 52.0 61.5 ± 1.8 in the health subjects and PAD patients, respectively. All nAChR clusters were innervated by the motor nerve terminal in the health subjects, whereas 8.6% of nAChR clusters were denervated in PAD Patients. These data indicate that the total nAChR area per nAChR cluster and the area of each discrete fragment are reduced and fragmented nAChR clusters are increased in PAD patients. Additionally, the denervation of nAChR clusters is increased in PAD patients. These results suggest that the neuromuscular transmission is compromised in PAD patients, which limits patients’ physical activities. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Withdrawal of cardiac vagal activity is associated with ventricular arrhythmias-related sudden cardiac death and high mortality in T2DM patients. Although vagal nerve stimulation (VNS) has emerged as a promising therapy for ventricular arrhythmias, VNS-induced off-target side effects due to a lack of organ specificity severely limit its prescription in the clinic. To avoid the limitations of the VNS, we employed an optogenetic technique that combines with a miniaturized bio-optoelectronic implant with genetic targeting strategies to achieve cardiac-specific vagal activation in T2DM rats. We hypothesize that optogenetic activation in cardiac vagal postganglionic (CVP) neurons can restore vagal control of cardiac function, and further reduce susceptibility to ventricular arrhythmias in T2DM. Rat T2DM was induced by a high-fat diet plus streptozotocin injection. AAV-channelrhodopsin-2 (ChR2, 2 μl, 5x1012 vg/ml), an excitatory light-sensitive opsin gene, was in vivo transfected into CVP neurons located in the atrioventricular ganglion (AVG). At three weeks after opsin gene (i.e., AAV-ChR2) transfection, continual optogenetic stimulation in CVP neurons was applied twice daily (10 Hz, 50% duty cycle, 5 mW for 1 hour) by illuminating a LED probe that is controlled and powered wirelessly in conscious rats. Our data from immunofluorescence staining showed that microinjection of AAV-ChR2 into the AVG induced expression of ChR2-mcherry in almost all CVP neurons. Optogenetic activation of CVP neurons resulted in a negative inotropic reaction on the left ventricular systolic pressure in a frequency-dependent manner in anesthetized rats. Data from spectral analysis of heart rate variability demonstrated that optogenetic stimulation gradually restored T2DM-reduced high-frequency power (an index of cardiac vagal activation) from one to three days after optogenetic therapy in vivo, whereas it has no effect on low-frequency power (an index of cardiac sympathetic activation). Additionally, data from 24-hour continuous ECG recording in conscious rats demonstrated that optogenetic stimulation in CVP neurons improved the T2DM-impaired heterogeneity of ventricular electrical activity, which was measured by evaluating ventricular arrhythmia-related ECG parameters at three days after optogenetic therapy in vivo. These data suggested that optogenetic activation in CVP neurons might be an effective intervention against cardiac vagal dysfunction-related ventricular arrhythmias in the T2DM state. This study was supported by the Great Plains IDeA-CTR Pilot Grant (to DZ), NIH-NHLBI (R01HL144146 to YLL), and AHA Career Development Award (851929 to DZ). This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

The ability to associate temporally segregated information and assign positive or negative valence to environmental cues is paramount for survival. Studies have shown that different basolateral amygdala (BLA) projections are potentiated following reward or punishment learning(1–7). However, we do not yet understand how valence specific information is routed to the BLA neurons with the appropriate downstream projections. Nor do we understand how to reconcile the subsecond timescales of synaptic plasticity(8–11) with the longer timescales separating the predictive cues from their outcomes. Here, we demonstrate that neurotensin (NT) neurons in the paraventricular nucleus of the thalamus (PVT) projecting to the BLA (PVT-BLA:NT) mediate valence assignment by exerting concentration-dependent modulation in BLA during associative learning. We found that optogenetic activation of the PVT-BLA:NT projection promotes reward learning, while PVT-BLA projection-specific Nt gene knockout augments punishment learning. Using genetically encoded calcium and NT sensors, we further revealed that both calcium dynamics within the PVT-BLA:NT projection and NT concentrations in the BLA are enhanced after reward learning and reduced after punishment learning. Finally, we showed that CRISPR-mediated knockout of the Nt gene in the PVT-BLA pathway blunts BLA neural dynamics and attenuates the preference to active behavioral strategies to reward and punishment predictive cues. Taken together, we have identified NT as a neuropeptide that signals valence in the BLA, and showed that NT is a critical neuromodulator that orchestrates positive and negative valence assignment in amygdala neurons by extending valence-specific plasticity to behaviorally-relevant timescales.

How plants adapt and diverge in extreme environments is a key question of plant evolution and ecology. Mangrove invasion of intertidal environments is facilitated by adaptive phenotypes such as aerial roots, salt-secreting leaf, and viviparity, and genomic mechanisms including whole genome duplication and transposable element number reduction. However, a number of mangroves lack these typical phenotypes. The question we ask is whether these phenotypically atypical mangroves also have distinct genomic features? The sibling mangrove species Lumnitzera littorea and Lumnitzera racemosa provide a model to study this question. We sequenced and assembled their genomes to chromosome level, together with a closely related species Combretum micranthum. While most mangroves have small genomes, the genomes of both Lumnitzera species are large (1443 and 1317 Mb) and carry a high proportion of repeat sequences (~75%). Moreover, Lumnitzera species have not undergone post-gamma whole-genome duplications. Their genome size increased mainly due to the expansion of repeat sequences in their ancestors. However, Lumnitzera genomes have reduced transposable elements by constraining the proliferation of new LTR-RTs. Meanwhile, the two species have more gene families contracted than expanded, and some gene families with reversed size change may underlie their differentiation in root morphology and local distribution. We identified 86 chromosomal inversions, five of which are measured between 6.5 and 12.8 megabases. A number of genes located in these inversions function in pigment biosynthesis, a process likely involved in flower colour differentiation between the Lumnitzera species. We conclude that the mangroves with atypical phenotypes also have atypical genomic evolution.

The progression of neurodegenerative disorders can lead to impaired neurotransmission; however, the role of pathogenic factors associated with these diseases and their impact on the structures and functions of neurotransmitters have not been clearly established. Here we report the discovery that conformational and functional changes of a native neuropeptide, somatostatin (SST), occur in the presence of copper ions, metal-free amyloid-β (Aβ) and metal-bound Aβ (metal-Aβ) found as pathological factors in the brains of patients with Alzheimer's disease. These pathological elements induce the self-assembly of SST and, consequently, prevent it from binding to the receptor. In the reverse direction, SST notably modifies the aggregation profiles of Aβ species in the presence of metal ions, attenuating their cytotoxicity and interactions with cell membranes. Our work demonstrates a loss of normal function of SST as a neurotransmitter and a gain of its modulative function against metal-Aβ under pathological conditions.