Social withdrawal and deficits in social cognition are hallmarks of Alzheimer's disease (AD). While early deficits in social behavior and memory have been documented in mouse AD models, they remain understudied in rat models. Early-stage AD is accompanied by dysfunction of parvalbumin-positive (PV+) interneurons, implicating their potential connection to early symptoms. In this study, we employed a 5-trial social memory task to investigate early deficits in social cognition in 6-month-old TgF344-AD male and female rats. We counted the number of PV+ interneurons and recorded local field potentials during social interactions in the hippocampal CA2 - a region critical for social information processing. Our results show decreased social interest and novelty preference in TgF344-AD male and female rats. However, reduced PV+ interneuron numbers were observed only in female rats and specific to the CA2 area. The electrophysiological recordings revealed reduced theta-gamma phase-amplitude coupling in the CA2 during direct social interactions. We conclude that deficits in social cognition accompany early-stage AD in TgF344-AD rats and are potentially linked to PV+ interneuron and brain oscillatory dysfunction in the CA2 region of the hippocampus.

• Klíčová slova
• Alzheimer's disease, CA2, Hippocampus, Parvalbumin-positive interneurons, Social memory, TgF344-AD,
• MeSH
• Alzheimerova nemoc * patofyziologie   patologie   metabolismus   MeSH
• hipokampální oblast CA2 * patofyziologie   metabolismus   patologie   MeSH
• interneurony * metabolismus   patologie   MeSH
• krysa rodu Rattus MeSH
• modely nemocí na zvířatech MeSH
• parvalbuminy * metabolismus   MeSH
• pohlavní dimorfismus MeSH
• potkani inbrední F344 MeSH
• potkani transgenní MeSH
• sociální chování * MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• parvalbuminy * MeSH

The potential link between the infections and the development of Alzheimer's disease (AD) has led to speculations about the role of various pathogens in triggering amyloid-β (Aβ) overproduction, possibly leading to AD onset. The globally distributed dog roundworm Toxocara canis was suggested to be a suitable candidate due to neurotropism of the larvae and infection chronicity. This study investigated whether chronic T. canis infection induces AD-like pathology in mice and whether Aβ is toxic to T. canis. BALB/c and APP/PS1 transgenic mice, which overproduce Aβ, were infected with T. canis L3 larvae and monitored for larval burden, Aβ accumulation, and behavioral changes. In vitro tests of recombinant Aβ toxicity against the larvae were also performed. Despite the presence of T. canis larvae in the central nervous system 8 and 16 weeks post-infection, no significant increase in Aβ concentration or AD-related behavioral alterations were observed. Aβ was detected on the surface and within the intestines of T. canis larvae, but in vitro exposure to recombinant Aβ did not affect larval viability or morphology. Our findings suggest that T. canis infection does not trigger AD-like pathology in mice, and Aβ does not act as an antiparasitic agent. This challenges the emerging hypothesis that chronic neurotoxocarosis infections may contribute to AD development.

TITLE: Absence de preuve de pathologie de la maladie d’Alzheimer chez les souris infectées par Toxocara canis. ABSTRACT: Le lien potentiel entre les infections et le développement de la maladie d’Alzheimer (MA) a suscité des spéculations sur le rôle de divers agents pathogènes dans le déclenchement de la surproduction de β-amyloïde (βA), pouvant conduire à l’apparition de la MA. Toxocara canis, un nématode du chien, répandu mondialement, a été suggéré comme un candidat potentiel en raison du neurotropisme de ses larves et de la chronicité de son infection. Cette étude examine si une infection chronique à T. canis induit une pathologie de type MA chez la souris et si la βA est toxique pour T. canis. Des souris transgéniques BALB/c et APP/PS1, qui surproduisent la βA, ont été infectées par des larves L3 de T. canis et la charge larvaire, l’accumulation de βA et les changements comportementaux ont été étudiés. Des tests in vitro de toxicité de la βA recombinante contre les larves ont également été réalisés. Malgré la présence de larves de T. canis dans le système nerveux central 8 et 16 semaines après l’infection, aucune augmentation significative de la concentration de la βA ni d’altération comportementale liée à la MA n’ont été observées. La βA a été détectée à la surface et dans les intestins des larves de T. canis, mais l’exposition in vitro à la βA recombinante n’a pas affecté la viabilité ou la morphologie des larves. Nos résultats suggèrent que l’infection à T. canis ne déclenche pas de pathologie de type MA chez la souris, et que la βA n’agit pas comme agent antiparasitaire. Cela remet en cause l’hypothèse émergente selon laquelle les infections chroniques par neurotoxocarose pourraient contribuer au développement de la MA.

• Klíčová slova
• Alzheimer’s disease, Amyloid-β, Infectious hypothesis, Neurotoxocarosis, Toxocara canis,
• MeSH
• Alzheimerova nemoc * patologie   parazitologie   etiologie   MeSH
• amyloidní beta-protein toxicita   metabolismus   analýza   MeSH
• larva MeSH
• modely nemocí na zvířatech MeSH
• myši inbrední BALB C MeSH
• myši transgenní MeSH
• myši MeSH
• psi MeSH
• střeva parazitologie   MeSH
• Toxocara canis * fyziologie   růst a vývoj   MeSH
• toxokaróza * komplikace   patologie   parazitologie   MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• myši MeSH
• psi MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• amyloidní beta-protein MeSH

OBJECTIVES: Decision-analytic models assessing the value of emerging Alzheimer's disease (AD) treatments are challenged by limited evidence on short-term trial outcomes and uncertainty in extrapolating long-term patient-relevant outcomes. To improve understanding and foster transparency and credibility in modeling methods, we cross-compared AD decision models in a hypothetical context of disease-modifying treatment for mild cognitive impairment (MCI) due to AD. METHODS: A benchmark scenario (US setting) was used with target population MCI due to AD and a set of synthetically generated hypothetical trial efficacy estimates. Treatment costs were excluded. Model predictions (10-year horizon) were assessed and discussed during a 2-day workshop. RESULTS: Nine modeling groups provided model predictions. Implementation of treatment effectiveness varied across models based on trial efficacy outcome selection (clinical dementia rating - sum of boxes, clinical dementia rating - global, mini-mental state examination, functional activities questionnaire) and analysis method (observed severity transitions, change from baseline, progression hazard ratio, or calibration to these). Predicted mean time in MCI ranged from 2.6 to 5.2 years for control strategy and from 0.1 to 1.0 years for difference between intervention and control strategies. Predicted quality-adjusted life-year gains ranged from 0.0 to 0.6 and incremental costs (excluding treatment costs) from -US$66 897 to US$11 896. CONCLUSIONS: Trial data can be implemented in different ways across health-economic models leading to large variation in model predictions. We recommend (1) addressing the choice of outcome measure and treatment effectiveness assumptions in sensitivity analysis, (2) a standardized reporting table for model predictions, and (3) exploring the use of registries for future AD treatments measuring long-term disease progression to reduce uncertainty of extrapolating short-term trial results by health-economic models.

• Klíčová slova
• Alzheimer’s disease, cross-validation, decision-analytic modeling, health-economic evaluation,
• MeSH
• Alzheimerova nemoc * ekonomika   farmakoterapie   terapie   MeSH
• analýza nákladů a výnosů * MeSH
• ekonomické modely MeSH
• kognitivní dysfunkce * ekonomika   farmakoterapie   MeSH
• kvalitativně upravené roky života MeSH
• lidé MeSH
• metody pro podporu rozhodování * MeSH
• progrese nemoci MeSH
• senioři MeSH
• Check Tag
• lidé MeSH
• senioři MeSH
• Publikační typ
• časopisecké články MeSH
• srovnávací studie MeSH

To investigate the impact of hyperbaric oxygen therapy (HBOT) on the cognitive function of mice with Alzheimer's disease (AD), while also identifying the cellular pathways associated with autophagy involved in the treatment. Twenty-four APP/PSl double transgenic mice were randomly assigned to either Group A or Group B, while another 24 C57 mice were randomly allocated to Group C or Group D. HBOT was administered to mice in Group B and Group D, and the Morris water maze test was used to assess changes in mice behavior. Histological examination using hematoxylin and eosin staining was conducted to observe pathological alterations in the hippocampus of the mice brain tissue. Polymerase chain reaction (PCR) was employed to analyze autophagy-related gene pathways in the hippocampus of the mice. Following HBOT, mice in Group B exhibited a significant reduction in escape latency and a notable increase in residence time within the target quadrant compared with Group A (P<0.05), as well as Group C and Group D (P<0.01). The hippocampal neurons in Group A and Group B mice exhibited disorganized arrangements, characterized by pyknosis and margination. Conversely, neurons in Group C displayed orderly arrangements, retaining intact structures with round nuclei demonstrating clear nuclear staining and normal morphology. The cellular morphology of mice in Group D remained unaffected. PCR analysis revealed no notable disparity in autophagy-related gene expression between Group A and Group C. However, the expression levels of five genes including Tgfb1, Mapk14, Bid, Atg7, and Akt1, were significantly elevated in Group B compared to Group A. HBOT has the potential to improve the cognitive function in mice modeled with AD. This improvement of cognitive function appears to be mediated by the up-regulation of autophagy-related genes, specifically Tgfb1, Mapk14, Bid, Atg7, and Akt1. These results indicate that HBOT may offer a therapeutic strategy for treating AD by enhancing autophagy mechanisms. Key words Alzheimer's disease, Autophagy, Hyperbaric oxygen, Morris water maze, PCR.

• MeSH
• Alzheimerova nemoc * terapie   metabolismus   genetika   psychologie   MeSH
• autofagie * fyziologie   MeSH
• hipokampus metabolismus   patologie   MeSH
• hyperbarická oxygenace * MeSH
• kognice * fyziologie   MeSH
• lidé MeSH
• modely nemocí na zvířatech MeSH
• myši inbrední C57BL * MeSH
• myši transgenní * MeSH
• myši MeSH
• signální transdukce * MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH

Berberine (BBR), a small molecule protoberberine isoquinoline alkaloid, is easy to cross the blood-brain barrier and is a potential drug for neurodegenerative diseases. Here, we explored the role and molecular mechanism of BBR in Alzheimer's disease (AD) progression. Weighted gene co-expression network analysis (WGCNA) was conducted to determine AD pathology-associated gene modules and differentially expressed genes (DEGs) were also identified. GO and KEGG analyses were performed for gene function and signaling pathway annotation. Cell counting kit-8 (CCK8) assay was applied to analyze cell viability. Immunofluorescence (IF) staining assay was conducted to measure the levels of polarization markers. The production of inflammatory cytokines was analyzed by enzyme-linked immunosorbent assay (ELISA). Reactive oxygen species (ROS) level and mitochondrial membrane potential (MMP) were detected using a ROS detection kit and a MMP Detection Kit (JC-1), respectively. AD pathology-associated DEGs were applied for GO function annotation and KEGG enrichment analysis, and the results uncovered that AD pathology was related to immune and inflammation. Lipopolysaccharide (LPS) exposure induced the M1 phenotype of microglia, and BBR suppressed LPS-induced M1 polarization and induced microglia toward M2 polarization. Through co-culture of microglia and neuronal cells, we found that BBR exerted a neuro-protective role by attenuating the injury of LPS-induced HMC3 on SH-SY5Y cells. Mechanically, BBR switched the M1/M2 phenotypes of microglia by activating PI3K-AKT signaling. In summary, BBR protected neuronal cells from activated microglia-mediated neuro-inflammation by switching the M1/M2 polarization in LPS-induced microglia via activating PI3K-AKT signaling. Key words Alzheimer's Disease, Berberine, Microglia polarization, Neuroinflammation, PI3K-AKT signaling.

• MeSH
• Alzheimerova nemoc * metabolismus   farmakoterapie   patologie   MeSH
• berberin * farmakologie   terapeutické užití   MeSH
• fosfatidylinositol-3-kinasy * metabolismus   MeSH
• lidé MeSH
• mikroglie * účinky léků   metabolismus   MeSH
• myši MeSH
• neuroprotektivní látky * farmakologie   MeSH
• polarita buněk účinky léků   MeSH
• protoonkogenní proteiny c-akt * metabolismus   MeSH
• signální transdukce * účinky léků   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• berberin * MeSH
• fosfatidylinositol-3-kinasy * MeSH
• neuroprotektivní látky * MeSH
• protoonkogenní proteiny c-akt * MeSH

Alzheimer's disease (AD), a leading cause of dementia worldwide, is a multifactorial neurodegenerative disorder characterized by amyloid-beta plaques, tauopathy, neuronal loss, neuro-inflammation, brain atrophy, and cognitive deficits. AD manifests as familial early-onset (FAD) with specific gene mutations or sporadic late-onset (LOAD) caused by various genetic and environmental factors. Numerous transgenic rodent models have been developed to understand AD pathology development and progression. The TgF344-AD rat model is a double transgenic model that carries two human gene mutations: APP with the Swedish mutation and PSEN-1 with delta exon 9 mutations. This model exhibits a complete repertoire of AD pathology in an age-dependent manner. This review summarizes multidisciplinary research insights gained from studying TgF344-AD rats in the context of AD pathology. We explore neuropathological findings; electrophysiological assessments revealing disrupted synaptic transmission, reduced spatial coding, network-level dysfunctions, and altered sleep architecture; behavioral studies highlighting impaired spatial memory; alterations in excitatory-inhibitory systems; and molecular and physiological changes in TgF344-AD rats emphasizing their age-related effects. Additionally, the impact of various interventions studied in the model is compiled, underscoring their role in bridging gaps in understanding AD pathogenesis. The TgF344-AD rat model offers significant potential in identifying biomarkers for early detection and therapeutic interventions, providing a robust platform for advancing translational AD research. Key words Alzheimer's disease, Transgenic AD models, TgF344-AD rats, Spatial coding.

• MeSH
• Alzheimerova nemoc * genetika   patologie   metabolismus   MeSH
• amyloidový prekurzorový protein beta genetika   metabolismus   MeSH
• krysa rodu Rattus MeSH
• lidé MeSH
• modely nemocí na zvířatech * MeSH
• mozek patologie   metabolismus   MeSH
• potkani inbrední F344 MeSH
• potkani transgenní * MeSH
• presenilin-1 genetika   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• amyloidový prekurzorový protein beta MeSH
• presenilin-1 MeSH

This study investigates the impact of combined special education and occupational therapy intervention on cognitive functions in Alzheimer's patients. Specifically, it evaluates changes measured by the Addenbrooke's Cognitive Examination (ACE-R) after six months compared to a control group receiving standard care. A longitudinal, controlled experiment was conducted with random assignment to experimental and control groups. The experimental group underwent three weekly interventions of 45-50 min over eight months in 2021. Cognitive functions were periodically assessed using ACE-R. Power analysis determined a sample size of 128 participants for adequate statistical power; the study included 60 participants (30 per group). Data were analyzed using non-parametric methods due to non-normal data distribution. The experimental group showed significant improvement in ACE-R scores compared to the control group. The mean difference in scores was 10.27 points (SD = 2.83) for the experimental group, indicating improved cognitive function, while the control group showed a mean decrease of 5.67 points (SD = 2.06). Statistical analysis confirmed significant differences between groups at both interim and final assessments (p < 0.001). The combined special education and occupational therapy intervention led to significant cognitive improvements in Alzheimer's patients compared to standard care. The study supports the efficacy of such interventions in enhancing cognitive functions, as evidenced by the substantial score increases in the experimental group.

• Klíčová slova
• Alzheimer disease, Cognitive function, Combined therapy, randomized controlled trial, Quality of life for older adults, Occupational therapy intervention, Special education intervention,
• MeSH
• Alzheimerova nemoc * rehabilitace   psychologie   patofyziologie   MeSH
• ergoterapie metody   MeSH
• kognice * fyziologie   MeSH
• lidé středního věku MeSH
• lidé MeSH
• longitudinální studie MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• výsledek terapie MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• randomizované kontrolované studie MeSH

BackgroundThe prevalence of Alzheimer's disease (AD) is increasing, and with it comes the demand for specialized services. Current information on the institutionalization of patients with AD is limited.ObjectiveTo determine the level of institutionalization among AD patients in the facilities of the Czech Republic and the Slovak Republic.MethodsA survey of the rate of institutionalization in facilities in the Czech Republic and Slovak Republic. The survey collects data on the institutionalization of patients suffering from AD in relation to the capacity of the facilities and the prevalence of the disease. Data were collected by representative quantitative survey, during years 2019-2021.ResultsPatients with AD occupy approximately 25% of the total capacities of institutions in the Czech and Slovak Republics. The rate of institutionalization of patients with AD is estimated at 20.5% in the Czech Republic and 24% in the Slovak Republic. This is more than the estimated worldwide rate of institutionalization of people with AD (16%) but less than the estimated rate of institutionalization of these patients in high-income countries (31%).ConclusionsAs the prevalence of AD increases, so do the demands for care. If there is no increase in institutional capacity, this growth will put more pressure on home care. In order to provide specialized care to as many patients as possible, emphasis must be placed on increasing the capacity of institutions.

• Klíčová slova
• Alzheimer's disease, dementia, inpatient care, institutionalization,
• MeSH
• Alzheimerova nemoc * epidemiologie   MeSH
• institucionalizace * statistika a číselné údaje   MeSH
• lidé MeSH
• prevalence MeSH
• průzkumy a dotazníky MeSH
• senioři MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• Geografické názvy
• Česká republika epidemiologie   MeSH
• Slovenská republika epidemiologie   MeSH

Maintaining cellular homeostasis by removing damaged and senescent mitochondria, a process termed mitophagy, is crucial in preventing Alzheimer's disease (AD) and represents a promising therapeutic target. Our previous research revealed altered mitophagy biomarkers, such as increased CSF and serum PINK1 and serum BNIP3L and decreased serum TFEB levels, indicating impaired autophagy-lysosomal degradation in the AD continuum. However, the role of autophagy/mitophagy in frontotemporal lobar degeneration (FTLD) remains unclear. This study investigated the biomarkers of autophagy/mitophagy and lysosomal biogenesis (PINK1, ULK1, BNIP3L, and TFEB) in biofluids (CSF and serum) from 308 biomarker-defined individuals across the FTLD continuum (FTLD-dementia, n = 29; FTLD-MCI, n = 33) and compared them with those across the AD continuum (MCI-AD, n = 100; AD-dementia, n = 100) and cognitively unimpaired (CU) controls (n = 46) recruited from Czech Brain Aging Study. Additionally, we compared the mitophagy biomarkers across different FTLD clinical subtypes (frontal, semantic and nonfluent variant) with CU, and explored the association between mitophagy biomarkers and clinical phenotypes of FTLD (biomarkers of tau, biomarkers of neurodegeneration, cognition and ATN profile).Our findings indicated a significantly lower CSF PINK1 and ULK1 levels in FTLD compared to AD, with FTLD dementia showing particularly low CSF PINK1 levels compared to AD-dementia. Conversely, CSF ULK1 levels were higher in FTLD-MCI compared to AD-dementia. Serum analyses revealed lower PINK1 and higher TFEB levels in FTLD dementia compared to AD dementia. This study provides compelling evidence of distinct alterations in autophagy/mitophagy biomarkers between FTLD and AD, indicating that these neurodegenerative diseases may affect the cellular waste disposal system through different pathways. This is the first study to explore mitophagy biomarkers in human CSF and serum in FTLD, opening avenues for further research and potential clinical applications.

• Klíčová slova
• Autophagy, Frontotemporal lobar degeneration, MAPT, Neurocognitive impairment, PINK1, TDP-43, TFEB,
• MeSH
• Alzheimerova nemoc * krev   patologie   mozkomíšní mok   MeSH
• autofagie * fyziologie   MeSH
• biologické markery * mozkomíšní mok   krev   MeSH
• frontotemporální lobární degenerace * patologie   mozkomíšní mok   krev   MeSH
• homolog Atg1 metabolismus   MeSH
• intracelulární signální peptidy a proteiny MeSH
• lidé středního věku MeSH
• lidé MeSH
• mitofagie * MeSH
• proteinkinasy metabolismus   krev   MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• biologické markery * MeSH
• homolog Atg1 MeSH
• intracelulární signální peptidy a proteiny MeSH
• proteinkinasy MeSH
• PTEN-induced putative kinase MeSH Prohlížeč
• ULK1 protein, human MeSH Prohlížeč

Alzheimer's disease (AD) is the most common form of dementia. Characterized by progressive neurodegeneration, AD typically begins with mild cognitive decline escalating to severe impairment in communication and responsiveness. It primarily affects cerebral regions responsible for cognition, memory, and language processing, significantly impeding the functional independence of patients. With nearly 50 million dementia cases worldwide, a number expected to triple by 2050, the need for effective treatments is more urgent than ever. Recent insights into the association between obesity, type 2 diabetes mellitus, and neurodegenerative disorders have led to the development of promising treatments involving antidiabetic and anti-obesity agents. One such novel promising candidate for addressing AD pathology is a lipidized analogue of anorexigenic peptide called prolactin-releasing peptide (palm11-PrRP31). Interestingly, anorexigenic and orexigenic peptides have opposite effects on food intake regulation, however, both types exhibit neuroprotective properties. Recent studies have also identified ghrelin, an orexigenic peptide, as a potential neuroprotective agent. Hence, we employed both anorexigenic and orexigenic compounds to investigate the common mechanisms underpinning their neuroprotective effects in a triple transgenic mouse model of AD (3xTg-AD mouse model) combining amyloid-beta (Aβ) pathology and Tau pathology, two hallmarks of AD. We treated 3xTg-AD mice for 4 months with two stable lipidized anorexigenic peptide analogues - palm11-PrRP31, and liraglutide, a glucagon-like peptide 1 (GLP-1) analogue - as well as Dpr3-ghrelin, a stable analogue of the orexigenic peptide ghrelin, and using the method of immunohistochemistry and western blot demonstrate the effects of these compounds on the development of AD-like pathology in the brain. Palm11-PrRP31, Dpr3-ghrelin, and liraglutide reduced intraneuronal deposits of Aβ plaque load in the hippocampi and amygdalae of 3xTg-AD mice. Palm11-PrRP31 and Dpr3-ghrelin reduced microgliosis in the hippocampi, amygdalae, and cortices of 3xTg-AD mice. Palm11-PrRP31 and liraglutide reduced astrocytosis in the amygdalae of 3xTg-AD mice. We propose that these peptides are involved in reducing inflammation, a common mechanism underlying their therapeutic effects. This is the first study to demonstrate improvements in AD pathology following the administration of both orexigenic and anorexigenic compounds, highlighting the therapeutic potential of food intake-regulating peptides in neurodegenerative disorders.

• Klíčová slova
• 3xTg-AD mice, Alzheimer’s disease, Anorexigenic peptide analogues, Neuroinflammation, Orexigenic peptide analogues,
• MeSH
• Alzheimerova nemoc * farmakoterapie   metabolismus   patologie   MeSH
• amyloidní beta-protein metabolismus   MeSH
• amyloidový prekurzorový protein beta genetika   metabolismus   MeSH
• ghrelin farmakologie   analogy a deriváty   terapeutické užití   metabolismus   MeSH
• hormon uvolňující prolaktin * analogy a deriváty   farmakologie   MeSH
• lidé MeSH
• liraglutid farmakologie   terapeutické užití   MeSH
• modely nemocí na zvířatech * MeSH
• myši inbrední C57BL MeSH
• myši transgenní * MeSH
• myši MeSH
• neuroprotektivní látky farmakologie   terapeutické užití   MeSH
• neurozánětlivé nemoci farmakoterapie   metabolismus   MeSH
• presenilin-1 genetika   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• amyloidní beta-protein MeSH
• amyloidový prekurzorový protein beta MeSH
• ghrelin MeSH
• hormon uvolňující prolaktin * MeSH
• liraglutid MeSH
• neuroprotektivní látky MeSH
• presenilin-1 MeSH