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The behavioral, pathological and therapeutic features of the triple transgenic Alzheimer's disease (3 x Tg-AD) mouse model strain

EXPERIMENTAL NEUROLOGY (2023)

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Summary: This study investigates the potential therapeutic effect of pantethine on cognitive deficits and pathology in a triple transgenic Alzheimer's disease (AD) mouse model. The results show that oral administration of pantethine improves spatial learning and memory ability, reduces anxiety, and mitigates the production of amyloid-beta, neuronal damage, and inflammation in the AD mice. Pantethine also reduces body weight, body fat, and cholesterol production by inhibiting specific signal pathways and expression of certain proteins.

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Summary: The pathophysiology of Alzheimer's disease involves the accumulation of amyloid-beta and hyperphosphorylated tau in the brain. Recent studies indicate that neurovascular cell alterations contribute to tau pathology and cell death. Tetramethylpyrazine nitrone (TBN) has been shown to have neuroprotective effects and targets A beta and tau pathologies, making it a potential treatment for AD.

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Myricetin improves pathological changes in 3xTg-AD mice by regulating the mitochondria-NLRP3 inflammasome-microglia channel by targeting P38 MAPK signaling pathway

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Summary: The study investigates the therapeutic effect of Myricetin on Alzheimer's disease (AD) and its potential mechanism of action. It is found that Myricetin protects against neurodegeneration by inhibiting the P38 MAPK signaling pathway, regulating mitochondria-NLRP3 inflammasome-microglia crosstalk, and reducing neuroinflammation. Myricetin shows promising potential as a drug candidate for AD treatment through targeting the P38 MAPK pathway.

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Age dependence of retinal vascular plexus attenuation in the triple transgenic mouse model of Alzheimer's disease

Hossein K. Nazari et al.

Summary: The study compared the impact of normal aging and AD progression on retinal vascular features in mice, revealing accelerated vascular changes in the SVP and DVP regions during AD progression. These findings suggest that parameters of the retinal vascular network may serve as markers for diagnosing and staging AD.

EXPERIMENTAL EYE RESEARCH (2022)

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JOTROL, a Novel Formulation of Resveratrol, Shows Beneficial Effects in the 3xTg-AD Mouse Model

Jessica L. Dennison et al.

Summary: JOTROL, a novel oral formulation of resveratrol, has higher bioavailability compared to non-formulated resveratrol. It has been found to be effective in the prevention and treatment of AD by regulating AD-related gene expression, inhibiting inflammatory genes, and regulating cytokine levels.

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Article Neurosciences

Low-Dose Radiation Therapy Reduces Amyloid Load in Young 3xTg-AD Mice

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Summary: This study found that low-dose radiation therapy (LD-RT) reduced amyloid load and possibly neuroinflammation markers in early-stage Alzheimer's disease, but did not impact tauopathy.

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Adiponectin Ameliorates Cognitive Behaviors and in vivo Synaptic Plasticity Impairments in 3xTg-AD Mice

Xu-Dong Yan et al.

Summary: This study found that adiponectin can ameliorate cognitive deficits in 3xTg-AD mice by improving synaptic plasticity impairments and alleviating neuroinflammation.

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Article Neurosciences

Fingolimod Rescues Memory and Improves Pathological Hallmarks in the 3xTg-AD Model of Alzheimer's Disease

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Summary: This study demonstrates that fingolimod may be a potential multimodal therapeutic for Alzheimer's disease, as it can reverse deficits in spatial working memory, alleviate inflammation in the brain, and reduce tau and APP levels in key brain regions.

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The effect of exercise on early sensorimotor performance alterations in the 3xTg-AD model of Alzheimer's disease

Sonja K. Bareiss et al.

Summary: Alzheimer's disease is associated with a decline in cognitive function as well as non-cognitive sensorimotor and psychomotor symptoms. While exercise is believed to be beneficial for AD, its effect on sensorimotor functions is not well understood. In this study, researchers found that exercise can improve sensorimotor function and reduce abnormal behavior in a mouse model of AD.

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Compromised Astrocyte Swelling/Volume Regulation in the Hippocampus of the Triple Transgenic Mouse Model of Alzheimer's Disease

Jana Tureckova et al.

Summary: This study reveals the impact of amyloid-beta toxicity and tau pathology on astrocyte swelling, volume recovery, and extracellular space diffusion in a mouse model of Alzheimer's disease. AD progression affects astrocyte ionic/neurotransmitter uptake, leading to enlarged extracellular space and increased obstacles. These changes may disrupt intercellular communication and contribute to cytotoxicity.

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被撤回的出版物: Neuroprotective Effects of Probiotic-Supplemented Diet on Cognitive Behavior of 3xTg-AD Mice (Retracted Article)

Chenxi Tan et al.

Summary: The study aimed to investigate the effects of a probiotic-supplemented diet on mouse models of Alzheimer's disease (AD). The results showed that the probiotic diet improved the learning and memory abilities of AD mice, enhanced spontaneous alternation accuracy, and regulated changes in the intestinal flora.

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Systematic Phenotyping and Characterization of the 3xTg-AD Mouse Model of Alzheimer's Disease

Dominic I. Javonillo et al.

Summary: Animal models are important for studying disease mechanisms and potential treatments, but the availability of numerous animal models presents challenges for Alzheimer's disease (AD) researchers. In this study, the 3xTg-AD mouse model was analyzed to understand the specific pathologies that develop at different ages and to comment on changes since its development 20 years ago. The study also compared the 3xTg-AD model with the 5xFAD model and found that plasma NfL is influenced by plaque burden. The results are freely available for researchers and demonstrate the usefulness of a standardized characterization pipeline for investigating and comparing different AD models.

FRONTIERS IN NEUROSCIENCE (2022)

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Alzheimer-like tau accumulation in dentate gyrus mossy cells induces spatial cognitive deficits by disrupting multiple memory-related signaling and inhibiting local neural circuit

Shihong Li et al.

Summary: The pathological accumulation of tau protein in mossy cells may induce spatial memory deficits resembling AD by inhibiting local neural network activity, revealing new pathogenesis and providing a mouse model for drug development.

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Amyloid β/PKC-dependent alterations in NMDA receptor composition are detected in early stages of Alzheimer′s disease

Carolina Ortiz-Sanz et al.

Summary: Research has shown that Aβ oligomers play a novel role in synaptic dysfunction in the early stages of Alzheimer's disease by modifying the contribution of NR2B to NMDAR composition and function through an integrin β1 and PKC-dependent pathway.

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Human tau accumulation promotes glycogen synthase kinase-3β acetylation and thus upregulates the kinase: A vicious cycle in Alzheimer neurodegeneration

Qiuzhi Zhou et al.

Summary: This study revealed a vicious cycle between tau hyperphosphorylation and GSK-3R activation through tau-mediated acetylation of GSK-3R. Inhibiting GSK-3R acetylation competitively improved cognitive impairment and AD-like pathologies.

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Wenping Lu et al.

Summary: This study found similar pathological features among aging, Alzheimer's disease, and perioperative neurocognitive disorders (PND), including altered mitochondrial homeostasis and dysregulated autophagy. Additionally, laparotomy may exacerbate cognitive deficits associated with independent neuronal inflammation, mitochondrial dysfunction, and neuronal loss. Dysregulation of PKC/PKR activity may be involved in the pathogenesis of these neurodegenerative diseases.

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Active Immunotherapy with 12-mer Aβ1-42-like Assembly Vaccine Shows Efficacy in Aged 3xTg-AD Mice

Hao Fang et al.

Summary: The novel recombinant chimeric vaccine showed significant immunogenicity and neuroprotective effects in AD mice, making it a promising candidate for the prophylaxis of Alzheimer's disease.

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Neuronal Aquaporin 1 Inhibits Amyloidogenesis by Suppressing the Interaction Between Beta-Secretase and Amyloid Precursor Protein

Jinsu Park et al.

Summary: AQP1 levels are elevated in the cerebral cortex during the early stages of AD, particularly in vulnerable neurons, and increase as aging progresses in AD mouse models. AQP1 appears to reduce A beta production by inhibiting the binding between BACE1 and APP.

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Remodeling of projections from ventral hippocampus to prefrontal cortex in Alzheimer's mice

Feng Xu et al.

Summary: Research showed that in 3xTg AD model mice, there is remodeling of the hippocampus-to-prefrontal cortex afferents and intracellular accumulation of A beta in BLA and PFC, leading to increased avoidance behavior.

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Loganin substantially ameliorates molecular deficits, pathologies and cognitive impairment in a mouse model of Alzheimer’s disease

Lulin Nie et al.

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Tetrahydrobiopterin Improves Recognition Memory in the Triple-Transgenic Mouse Model of Alzheimer's Disease, Without Altering Amyloid-β and Tau Pathologies

Hortense Fanet et al.

Summary: Research shows potential benefits of BH4 administration in improving cognitive symptoms and metabolic disorders in triple-transgenic mice model of Alzheimer's disease, without altering classical neuropathology.

JOURNAL OF ALZHEIMERS DISEASE (2021)

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Article Neurosciences

PICALM mRNA Expression in the Blood of Patients with Neurodegenerative Diseases and Geriatric Depression

Hiroshi Kumon et al.

Summary: This study found that PICALM mRNA expression in human blood was higher in patients with AD but lower in patients with PD, suggesting it may serve as a useful biomarker for differentiating neurodegenerative diseases and geriatric MDD.

JOURNAL OF ALZHEIMERS DISEASE (2021)

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Article Neurosciences

Partial Inhibition of Mitochondrial Complex I Reduces Tau Pathology and Improves Energy Homeostasis and Synaptic Function in 3xTg-AD Mice

Andrea Stojakovic et al.

Summary: Treatment with CP2 can improve cognitive function, synaptic protein levels, glucose metabolism, and energy homeostasis in 3xTg-AD mice, especially restoring synaptic activity in female mice. This suggests that targeting mitochondria with specific MCI inhibitors could be a promising strategy for treating Alzheimer's disease.

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Design, synthesis and biological evaluation of harmine derivatives as potent GSK-3β/DYRK1A dual inhibitors for the treatment of Alzheimer's disease

Wenwu Liu et al.

Summary: Harmine derivatives were designed, synthesized, and evaluated as dual GSK-3 beta/DYRK1A inhibitors, showing promising activity against both targets. Compound ZDWX-25 exhibited potent inhibitory effects on GSK-3 beta and DYRK1A, with IC50 values of 71 and 103 nM, respectively. These compounds have the potential to be promising candidates for Alzheimer's disease treatment.

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Aberrant role of ALK in tau proteinopathy through autophagosomal dysregulation

Jisu Park et al.

Summary: The study reveals that aberrantly activated anaplastic lymphoma kinase (ALK) is a key factor contributing to the pathology of Alzheimer's disease (AD), by inducing abnormal accumulation of tau protein and causing dysfunction in neurons. The research demonstrates that ALK disrupts autophagosome maturation, leading to tau accumulation and aggregation, ultimately resulting in neuronal dysfunction in AD.

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Changes in the brain transcriptome after DNA Aβ42 trimer immunization in a 3xTg-AD mouse model

Doris Lambracht-Washington et al.

Summary: DNA Aβ42 immunization in 3xTg-AD mice showed reduced amyloid and tau pathology, improved nest building activity, and increased survival rate. The upregulated genes involved in inflammatory pathways in AD mice were downregulated after immunization, while the expression of genes related to neuronal pathways were restored to wild-type levels in immunized mice. The complex immune response after DNA Aβ42 immunization suggests a move towards disease prevention beyond the amyloid hypothesis.

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Differential effects of chronic immunosuppression on behavioral, epigenetic, and Alzheimer's disease-associated markers in 3xTg-AD mice

Minesh Kapadia et al.

Summary: Immunosuppression in 3xTg-AD mice prevented certain AD pathology features in males and maintained AD-like phenotype in females. This suggests a potential key role of autoimmunity in the pathogenesis of AD.

ALZHEIMERS RESEARCH & THERAPY (2021)

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Diffusion MRI detects basal forebrain cholinergic abnormalities in the 3xTg-AD mouse model of Alzheimer's disease

Maria Fatima Falangola et al.

Summary: This study found significant differences in dMRI values in the BF of 2-month-old 3xTg-AD mice compared to normal control mice, as well as age-related changes between 2 and 8 months, including a decrease in fractional anisotropy and axial diffusivity, and an increase in radial kurtosis. These dMRI changes likely reflect the complex aging and pathological microstructural changes described in this region, and could serve as potential in vivo biomarkers for AD disease progression.

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The 4-(Phenylsulfanyl) butan-2-one Improves Impaired Fear Memory Retrieval and Reduces Excessive Inflammatory Response in Triple Transgenic Alzheimer's Disease Mice

Peeraporn Varinthra et al.

Summary: Alzheimer's disease is characterized by excessive inflammatory response and memory impairment, with a compound 4-(phenylsulfanyl) butan-2-one (4-PSB-2) showing promising therapeutic effects in enhancing fear memory retrieval and synaptic transmission efficiency.

FRONTIERS IN AGING NEUROSCIENCE (2021)

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Losartan Improves Memory, Neurogenesis and Cell Motility in Transgenic Alzheimer's Mice

Henning Johannes Drews et al.

Summary: ARBs have shown neuroprotective benefits in AD models, with variable effects on memory deficits, cholinergic activity, neurogenesis, and A beta clearance. Systemic administration of losartan resulted in decreased A beta plaques, A beta 42, and inflammatory cytokines, while improving neurogenesis and astrocyte motility. Therapeutic features of losartan appear independent of delivery route.

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Aminopeptidase A contributes to biochemical, anatomical and cognitive defects in Alzheimer's disease (AD) mouse model and is increased at early stage in sporadic AD brain

Audrey Valverde et al.

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Liangmiao Wu et al.

Summary: The novel compound MN-08 was found to inhibit Aβ accumulation, prevent neuronal and dendritic spine loss, and improve cognitive deficits in mouse models of AD. MN-08 also demonstrated the ability to antagonize NMDA receptors and prevent neuronal loss in vitro. These findings suggest that MN-08 could be a promising therapeutic agent for AD.

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Systematic phenotyping and characterization of the 5xFAD mouse model of Alzheimer's disease

Stefania Forner et al.

Summary: Mouse models of human diseases are crucial for studying pathogenic mechanisms and testing interventions. To effectively evaluate new therapeutic approaches, it is important to identify the most appropriate model and age. In this study, a detailed phenotypic characterization of the 5xFAD model was conducted to provide insights into age-related pathology.

SCIENTIFIC DATA (2021)

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Retinoid X receptor activation promotes re-myelination in a very old triple transgenic mouse model of Alzheimer's disease

Daniel F. Santos-Gil et al.

Summary: Research indicates that Bexarotene can promote the expression of oligodendrocyte progenitor cells in an AD mouse model, increase the number of mature oligodendrocytes, and facilitate remyelination, which may contribute to cognitive improvement.

NEUROSCIENCE LETTERS (2021)

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Neuropathology of the Brainstem to Mechanistically Understand and to Treat Alzheimer's Disease

Agoston Patthy et al.

Summary: Alzheimer's disease (AD) is a devastating neurodegenerative disorder for which an effective therapy has yet to be found. Research suggests that early damage to the ascending monoaminergic system in the brainstem may be an early sign and potential trigger of AD. In addition, cortical malfunction and local neurohistopathology are also related to the progression of AD.

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Blocking microglial activation of reactive astrocytes is neuroprotective in models of Alzheimer's disease

Jong-Sung Park et al.

Summary: Alzheimer's disease is the most common cause of age-related dementia, with neuroinflammation playing a critical role in disease progression. Targeting microglia and astrocytes could provide potential therapies for slowing down neurodegeneration in AD.

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Age and gender differences for the behavioral phenotypes of 3xTg alzheimer's disease mice

Tanita Pairojana et al.

Summary: The study found that performing TFC tests on male 3xTg-AD mice is optimal for studying memory performance in AD. Sensory and locomotor functions in 3xTg-AD mice of both genders appear normal before 6 months, but decline in fear memory afterwards. There are significant differences in contextual and cued memory between control and 3xTg-AD male mice, making them ideal for evaluating treatment effects.

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Neurotrophic Treatment Initiated During Early Postnatal Development Prevents the Alzheimer-Like Behavior and Synaptic Dysfunction

Wei Wei et al.

Summary: Alzheimer's disease is characterized by cognitive impairment and loss of synaptic plasticity, and early treatment with P021 during development can prevent cognitive dysfunction and ameliorate synaptic protein deficit in AD mouse models.

JOURNAL OF ALZHEIMERS DISEASE (2021)

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3 x Tg-AD Mice Overexpressing Phospholipid Transfer Protein Improves Cognition Through Decreasing Amyloid-β Production and Tau Hyperphosphorylation

Wen-Zhi Wang et al.

Summary: The study demonstrates that PLTP overexpression has a protective effect on cognitive dysfunction and pathological changes in 3 x Tg-AD mice, possibly achieved through inhibiting A beta production and tau phosphorylation.

JOURNAL OF ALZHEIMERS DISEASE (2021)

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Intranasal Paclitaxel Alters Alzheimer's Disease Phenotypic Features in 3xTg-AD Mice

Donna J. Cross et al.

Summary: Intranasally administered microtubule-stabilizing drugs, specifically paclitaxel, have shown promise in altering the phenotypic progression of Alzheimer's disease in 3xTg-AD mice. These drugs can increase axonal transport rates, reduce phospho-tau containing neurons, improve performance in behavioral tests, and decrease anxiety-related behaviors.

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Bis(ethylmaltolato)oxidovanadium (IV) alleviates neuronal apoptosis through regulating peroxisome proliferator-activated receptor γ in a triple transgenic animal model of Alzheimer's disease

Zhijun He et al.

Summary: ER stress is a critical factor in neuronal apoptosis and AD progression, with PPAR gamma regulation being a promising therapeutic target. Vanadium compounds like BEOV have shown potential in alleviating ER stress and apoptosis in AD models through PPAR gamma modulation. Cotreatment with a PPAR gamma antagonist effectively blocked the neuroprotective effects of BEOV, indicating the key role of PPAR gamma-dependent signaling in protecting against ER stress and neuronal apoptosis in AD.

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Group 2 innate lymphoid cells are numerically and functionally deficient in the triple transgenic mouse model of Alzheimer's disease

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Limiting RyR2 open time prevents Alzheimer's disease-related deficits in the 3xTG-AD mouse model

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Distinct inflammatory phenotypes of microglia and monocyte-derived macrophages in Alzheimer's disease models: effects of aging and amyloid pathology

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Sodium selenate activated Wnt/β-catenin signaling and repressed amyloid-β formation in a triple transgenic mouse model of Alzheimer's disease

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Recent Progress in Alzheimer's Disease Research, Part 2: Genetics and Epidemiology

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Factors underlying cognitive decline in old age and Alzheimer's disease: the role of the hippocampus

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Mechanism of Oxidative Stress and Synapse Dysfunction in the Pathogenesis of Alzheimer's Disease: Understanding the Therapeutics Strategies

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Tau Protein Hyperphosphorylation and Aggregation in Alzheimer's Disease and Other Tauopathies, and Possible Neuroprotective Strategies

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Perirhinal cortex lesions impair tests of object recognition memory but spare novelty detection

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Selective deletion of forebrain glycogen synthase kinase 3β reveals a central role in serotonin-sensitive anxiety and social behaviour

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Physical Exercise Protects Against Alzheimer's Disease in 3xTg-AD Mice

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Endogenous Aβ causes cell death via early tau hyperphosphorylation

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Intraneuronal β-Amyloid Accumulation in the Amygdala Enhances Fear and Anxiety in Alzheimer's Disease Transgenic Mice

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Sex differences in β-amyloid accumulation in 3xTg-AD mice: Role of neonatal sex steroid hormone exposure

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Synergistic Interactions between Aβ, Tau, and α-Synuclein: Acceleration of Neuropathology and Cognitive Decline

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Quantitative and Mechanistic Studies of A beta Immunotherapy

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Triple-Transgenic Alzheimer's Disease Mice Exhibit Region-Specific Abnormalities in Brain Myelination Patterns Prior to Appearance of Amyloid and Tau Pathology

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Review Neurosciences

Heterogeneity of Microglial Activation in the Innate Immune Response in the Brain

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Age-dependent phenotypic characteristics of a triple transgenic mouse model of Alzheimer disease

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Detailed immunohistochemical characterization of temporal and spatial progression of Alzheimer's disease-related pathologies in male triple-transgenic mice

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Females exhibit more extensive amyloid, but not tau, pathology in an Alzheimer transgenic model

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Intraneuronal β-amyloid aggregates, neurodegeneration, and neuron loss in transgenic mice with five familial Alzheimer's disease mutations:: Potential factors in amyloid plaque formation

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Up-regulation of microglial CD11b expression by nitric oxide

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Temporal profile of amyloid-β (Aβ) oligomerization in an in vivo model of Alzheimer disease -: A link between Aβ and tau pathology

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White matter lesions are prevalent but differentially related with cognition in aging and early Alzheimer disease

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Lipopolysaccharide-induced inflammation exacerbates tau pathology by a cyclin-dependent kinase 5-mediated pathway in a transgenic model of Alzheimer's disease

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Intraneuronal Aβ causes the onset of early Alzheimer's disease-related cognitive deficits in transgenic mice

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Triple-transgenic model of Alzheimer's disease with plaques and tangles:: Intracellular Aβ and synaptic dysfunction

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Astrocytes accumulate Aβ42 and give rise to astrocytic amyloid plaques in Alzheimer disease brains

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Amyloid deposition precedes tangle formation in a triple transgenic model of Alzheimer's disease

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