PMCID string | Title string | Sentences string |
|---|---|---|
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Schematic representation of signaling pathways common to AD and DM induced by GLP-1R agonism. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | These include AMPK, PI3K/AKT, CaMKK2-AMPK, NF-κB, insulin/IGF-1 R and the mitochondrial signaling pathway. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Insulin resistance in the brain perpetuates neuroinflammation, tau hyperphosphorylation, and amyloid pathology in AD and is therefore a driver of neurodegenerative disease (Hölscher, 2019). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | This has led some researchers to refer to AD as “type 3 diabetes” because of the similarities between the impaired brain insulin signaling observed in AD and the insulin resistance observed in T2DM (see below) (de la Monte, 2014; Steen et al., 2005). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | However, this nomenclature has been controversial, with some scholars arguing that categorizing AD as “type 3 diabetes” may be conceptually misleading (Talbot and Wang, 2014; Li et al., 2024). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | The traditional classification of DM is mainly based on abnormalities in insulin secretion and action, such as type 1 DM due to an absolute lack of insulin secretion and T2DM due to insulin resistance and relative insulin deficiency. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | However, the inclusion of abnormal insulin metabolism in the brain as part of “type 3 diabetes” is a break from conventional wisdom and therefore has not yet been agreed upon in the academic community. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Firstly, some people believe that cerebral insulin resistance in patients with AD may not be insulin resistance in the true sense of the word but may instead arise from dysfunctional insulin transport across the BBB and that this transport defect may be caused by abnormal BBB function indirectly resulting from peripheral insulin resistance (Arnold et al., 2018). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Second, existing animal models have significant limitations. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Although rodent models provide important tools for AD research, it is difficult for these models to fully simulate the complex pathophysiological processes of human AD because of the significant differences in brain structure, metabolic characteristics, and immune responses between humans and experimental animals (Qian et al., 2024). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | However, abnormal desensitization of insulin signaling has been observed in the brain tissue of patients with AD even in the absence of DM (Frölich et al., 1998). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Multiple parallels between impaired brain insulin signaling in AD and insulin resistance in T2DM have been reported. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Insulin and insulin-like growth factor-1 (IGF-1) play important roles in cognitive performance, neurological function, and the control of neurogenesis and synaptogenesis (Choi et al., 2025). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Insulin-degrading enzymes (IDEs) are enzymes used to break down insulin and IGF-1, removing Aβ40 and Aβ42 monomers but not affecting Aβ oligomers or fibers (Kemeh and Lazo, 2023). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | In an insulin-resistant milieu, insulin may competitively inhibit IDE, which impedes the degradation of Aβ proteins, increases their neurotoxicity, and contributes to the onset of AD (Scherer et al., 2021; Ochiai et al., 2021). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | In the state of brain insulin resistance, insulin signaling pathways such as the PI3K/Akt pathway become abnormal, and abnormalities in insulin signaling pathways lead to a decrease in Aβ clearance, which promotes Aβ deposition (Zheng and Wang, 2021). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | In addition, brain insulin resistance affects tau metabolism and promotes the hyperphosphorylation of tau proteins, tau protein aggregation, the formation of paired helical filaments, and the further formation of NFTs (Mohandas et al., 2009). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | GLP-1, as an insulin-promoting hormone, has functional and growth factor properties similar to those of insulin and IGF-1 (Bhalla et al., 2022). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | GLP-1R, as its receptor, can bind to GLP-1 to exert its growth factor effects. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | In addition, Aβ has a tertiary structure similar to that of insulin, peripheral Aβ acts as a negative regulator of insulin secretion, and there can be interactions between Aβ and insulin signaling (You et al., 2022). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Brain insulin resistance is an important pathogenetic feature of AD and is mediated primarily by impaired insulin signaling (Sêdzikowska and Szablewski, 2021). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | In a study using the GLP-1R agonist liraglutide, its ability to reverse cognitive deficits in an AD model and its potential neuroprotective mechanisms were identified. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Liraglutide not only blocks insulin receptor and synaptic loss in the brain but also reverses memory impairment induced by AD-associated Aβ oligomers, suggesting that GLP-1R activation may be used to protect brain insulin receptors and synapses in AD (Batista et al., 2018). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | In addition, GLP-1R stimulation activates insulin signaling pathways and regulates gene expression, decreasing systemic insulin resistance and brain insulin resistance in patients with AD (Dahiya et al., 2025). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Moreover, because GLP-1R is expressed throughout the body, stimulation with a GLP-1R agonist or indirectly with a DPP-IV inhibitor can have a broad systemic effect on systemic metabolism, which, in turn, ameliorates peripheral and central insulin resistance in AD and MD (Athauda and Foltynie, 2016). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Therefore, it is reasonable to believe that GLP-1R is a potential link between these two diseases. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | AD and DM are significantly associated with neuroinflammatory mechanisms. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Chronic low-grade inflammation is a common pathological feature of both: metabolic disturbances in patients with DM induce the release of peripheral inflammatory factors, and these inflammatory factors pass through the compromised BBB into the central nervous system (CNS), activating microglia and astrocytes and triggering a neuroinflammatory cascade response, which in turn promotes Aβ deposition in AD and tau protein hyperphosphorylation (Sebastian Monasor et al., 2020; Chen et al., 2024). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | In addition, obesity-associated adipose tissue inflammation further exacerbates CNS inflammation, creating a vicious cycle of “metabolism–inflammation–neurodegeneration” (Chen et al., 2024; Wong et al., 2024). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | GLP-1R plays a multidimensional role in regulating neuroinflammation. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Firstly, through a systematic review and network meta-analysis, researchers have assessed the effects of GLP-1R agonists on neuroinflammation and reported that, compared with placebo, GLP-1R agonists significantly reduce the levels of neuroinflammatory markers, such as TNF-α and interleukin-1β (Urkon et al., 2025; Zhang et al., 2022; Tseng et al., 2025). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Second, GLP-1R activation enhances neurovascular coupling function, improves cerebral blood flow and repairs BBB integrity, blocking the penetration of peripheral inflammatory factors into the center (Wong et al., 2024). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Preclinical studies have also revealed that dual agonists of GLP-1R and glucose-dependent insulinotropic polypeptide receptor (GIPR) have synergistic anti-inflammatory and neuroprotective effects, suggesting the potential advantages of multitargeting strategies (Yuan et al., 2024). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | GLP-1R-targeted therapies have now expanded from metabolic diseases to AD. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | A team of researchers developed a nanostructure-based GLP-1R agonist capable of crossing the BBB that significantly attenuated neuroinflammation and memory loss in an Aβ peptide-induced mouse model of AD by inhibiting the inflammatory responses of microglia and astrocytes (Zhao et al., 2022). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | These findings not only reveal the potential of GLP-1R as a common therapeutic target for AD and DM but also provide a theoretical basis for the development of novel therapies based on the “metabolic–immune–neurological” axis. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Chronic hyperglycemia in patients with T2DM leads to peripheral insulin resistance, whereas impaired insulin signaling pathways in the brains of patients with AD lead to “brain insulin resistance,” both of which are closely related to mitochondrial dysfunction and OS (Du et al., 2022; Zhang et al., 2023). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Mitochondria are the primary site of energy metabolism and reactive oxygen species (ROS) production. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Hyperglycemia exacerbates mitochondrial electron transport chain (ETC) dysfunction and increases ROS production through advanced glycation end products and inflammatory pathways (Zhang et al., 2023; Caturano et al., 2023). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Overproduction of ROS triggers OS (Luna-Marco et al., 2023). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Interestingly, defects in mitochondrial energy metabolism are also present in the brains of patients with AD, leading to neuronal apoptosis and Aβ deposition, which increases ROS production by interfering with mitochondrial calcium homeostasis and ETC function; the hyperphosphorylation of tau proteins leads to the disruption of microtubule structure and affects mitochondrial axonal transport, exacerbating the neuronal energy crisis (Meng et al., 2024). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Activated microglia in patients with AD release proinflammatory factors, which further promote ROS production, creating a vicious cycle of neuroinflammation and mitochondrial dysfunction (Qian et al., 2025). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | GLP-1R can restore the mitochondrial membrane potential, promote ATP production, and reduce ROS production by activating the cAMP/PKA pathway (Signorile et al., 2022). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | In addition, activation of GLP-1R regulates mitochondrial over fission by the cAMP/PKA pathway while improving mitochondrial function in Aβ-treated astrocytes and ameliorating pathological lesions in AD (Xie et al., 2021). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Clinical studies have shown that GLP-1R reduces ROS levels, the mitochondrial membrane potential and mitochondrial apoptosis in patients with diabetes (Durak and Turan, 2023; Wang et al., 2021), as well as alleviating levels of OS and attenuating low-grade inflammation (Zhang et al., 2018). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | GLP-1R reduces oxidative damage accumulation by modulating autophagy-related proteins and scavenging damaged mitochondria while increasing superoxide dismutase (SOD) and glutathione peroxidase activities, reducing the generation of lipid peroxidation products, inhibiting the NF-κB signaling pathway, and decreasing proinflammatory factor expression to reduce neuroinflammation (Ma et al., 2018; Lin et al., 2021). |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | In conclusion, GLP-1R plays important roles in mitochondrial dysfunction and OS in AD and DM. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | The treatment of AD faces serious challenges, and the incidence of this disease is increasing every year, placing a heavy burden on global health. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Despite the never-ending exploration of AD, our understanding of the disease remains limited, especially in terms of etiology and pathogenesis. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Recent studies suggest that GLP-1R may be an important link between DM and AD. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Evidence suggests that GLP-1R agonists, initially developed for the treatment of DM, have therapeutic potential in the management of AD because of their multifaceted mechanism of action. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | GLP-1R agonists exhibit neuroprotective effects in AD, including anti-inflammatory effects, modulation of Aβ deposition and clearance, improved insulin signaling, and attenuation of OS. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | The intersection between DM and AD further highlights the shared pathophysiological mechanisms, particularly the disruption of insulin signaling pathways in the brain. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | This disruption is referred to as “type 3 diabetes” and is characterized by neuroinflammation, cognitive deficits, and amyloid pathology, which are common to both DM and AD. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | GLP-1R may ameliorate these conditions by improving insulin signaling and reducing insulin resistance in the brain. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Although GLP-1R agonists have yielded promising results in animal models, AD transgenic mice do not fully mimic the complex pathology of human AD, and there are still some challenges in translating them into effective AD therapies. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | For example, limitations in BBB penetration efficiency allow for limited distribution in the CNS, which may affect efficacy. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Current studies suggest that peripherally administered GLP-1RA has low concentrations in the cerebrospinal fluid, and higher doses or improved delivery systems (e.g., nanoparticles, liposome encapsulation) may be needed to increase brain exposure. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | In addition, there are potential risks and limitations associated with GLP-1R therapy. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Most GLP-1R agonists have gastrointestinal side effects, including nausea, vomiting, diarrhea and constipation, which may be more pronounced in elderly patients with AD and affect treatment compliance. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Whether long-term use leads to risks such as hypoglycemia and thyroid C-cell hyperplasia remains to be further evaluated. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | However, novel drug delivery systems or formulations may be able to reduce the risk of gastrointestinal side effects and hypoglycemia. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | With the in-depth theory of the gut–brain GLP-1R axis, the breakthrough of new material technology and the rapid development of AI-assisted drug design, GLP-1R-related research has also ushered in new opportunities. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | An in-depth analysis of the signaling mechanism of GLP-1R in the gut–brain GLP-1R axis is needed to aid in developing smarter new material delivery systems to achieve precise targeting and long-lasting release of GLP-1R agonists. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Moreover, AI technology can be used to accelerate the design and screening of novel GLP-1R agonists to promote personalized therapy. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | In conclusion, GLP-1R signaling represents a promising therapeutic strategy that bridges the treatment of DM and AD. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Its potential to modulate metabolic and neuroprotective pathways offers hope for the development of new therapies that could improve the prognosis of patients with both diseases. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | GLP-1R is not only a key target for metabolic regulation but also a bridge between metabolism and the nervous system. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | With further research and technological advances, GLP-1R agonists are expected to become the core drugs for the treatment of AD and DM. |
PMC12328308 | GLP-1R as a potential link between diabetes and Alzheimer’s disease | Future studies should continue to explore the dual mechanism of action of GLP-1R in metabolism and the nervous system, especially its potential applications at the intersection of AD and DM. |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | Alzheimer’s disease (AD) was a progressive neurodegenerative disorder characterised by an insidious onset and gradual cognitive decline. |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | It remained a significant global health challenge. |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | Methylparaben (MEP), a preservative commonly used in cosmetics and food processing, had been associated with the development and progression of AD. |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | First, we acquired the initial three-dimensional (3D) structure of MEP from PubChem (CID: 7456), followed by structural optimization via energy minimization using Chem3D software to complete its 3D structural characterisation. |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | This was followed by systematic target prediction across the SwissTargetPrediction, SEA, GeneCards and OMIM databases. |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | We then constructed protein-protein interaction (PPI) networks using STRING and visualised them in Cytoscape to identify core targets. |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | Molecular docking simulations using CB-Dock2 elucidated the binding affinities between MEP and the key proteins. |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | Experimental validation combined Gene Expression Omnibus (GEO) database analysis with quantitative reverse transcription polymerase chain reaction (qRT-PCR) to quantify transcriptional changes in SK-N-SH neural cells. |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | A total of 153 potential targets associated with MEP and AD were identified. |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | Ten core targets were determined through screening using the STRING platform and Cytoscape software, including HIF1A, IGF1R, PDGFRB, PTK2, VCAM1, CXCL12, ERBB2, ESR1, JAK2 and BCL2L1. |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | Furthermore, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses revealed that the core MEP targets in AD primarily concentrate on the following key signalling pathways: Neuroactive ligand-receptor interactions, EGFR tyrosine kinase inhibitor resistance, HIF-1 signalling pathway and gamma-aminobutyric acid (GABA) synapse. |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | Molecular docking simulations using CB-Dock2 confirmed a high binding affinity between MEP and these core targets. |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | To investigate the mechanism of action of MEP, we validated the findings using clinical datasets and the human neuroblastoma cell line SK-N-SH. |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | Upregulation of ten transcriptional expressions was observed, suggesting that MEP might influence cognitive function in patients with AD. |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | This study elucidated the potential molecular mechanisms of MEP in the progression of Alzheimer’s disease-related tau pathology, offering new insights for the prevention and intervention of degenerative diseases that might be triggered by excessive exposure to MEP environments. |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | Alzheimer’s disease (AD) was recognised as the most prevalent form of dementia. |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | It was a progressive neurodegenerative disorder that poses a significant challenge to global public health in contemporary society . |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | This devastating condition was characterised by a gradual deterioration of cognitive function, persistent memory impairment and a progressive loss of independence when performing daily activities. |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | It profoundly compromised patients’ quality of life and imposes a substantial socio-economic burden on affected families . |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | According to the latest estimates from the World Health Organization (WHO), the global prevalence of AD currently affected approximately 50 million individuals. |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | Epidemiological projections indicated that this figure was likely to double by 2050 . |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | These staggering statistics highlighted the significant social and economic burdens that were expected to emerge in the coming decades. |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | The etiopathogenesis of AD was characterized by its multifactorial nature, involving an intricate interplay between genetic predisposition, environmental determinants, and lifestyle factors . |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | Contemporary research had established that the hallmark neuropathological features of AD primarily include the cerebral accumulation of β-amyloid plaques and the formation of neurofibrillary tangles composed of hyperphosphorylated tau proteins . |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | These pathological alterations precipitated neuronal apoptosis and synaptic dysfunction, ultimately culminating in progressive cognitive deterioration . |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | Furthermore, emerging evidence highlighted the critical role of neuroinflammation, oxidative stress mechanisms, and blood-brain barrier dysfunction in accelerating AD progression . |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | Numerous studies had also indicated that a healthy diet is a key factor in reducing the risk of Alzheimer’s disease . |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | Methylparaben (MEP) was a compound of particular interest in this context, given its status as a ubiquitous environmental endocrine disrupter. |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | It was widely used as a preservative in personal care products, pharmaceuticals and food formulations. |
PMC12829224 | Integrating machine learning and experiments to elucidate the potential molecular mechanisms of methylparaben-induced Alzheimer’s disease: evidence from a Tau hyperphosphorylation cell model | It also occurred naturally in various fruits and vegetables . |
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