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  1. Article ; Online: Microdose lithium improves behavioral deficits and modulates molecular mechanisms of memory formation in female SAMP-8, a mouse model of accelerated aging.

    Pereira, Arthur Antonio Ruiz / Pinto, Alessandra Macedo / Malerba, Helena Nascimento / Toricelli, Mariana / Buck, Hudson Sousa / Viel, Tania Araujo

    PloS one

    2024  Volume 19, Issue 4, Page(s) e0299534

    Abstract: Alzheimer's disease (AD) is the most common neuronal disorder that leads to the development of dementia. Until nowadays, some therapies may alleviate the symptoms, but there is no pharmacological treatment. Microdosing lithium has been used to modify the ...

    Abstract Alzheimer's disease (AD) is the most common neuronal disorder that leads to the development of dementia. Until nowadays, some therapies may alleviate the symptoms, but there is no pharmacological treatment. Microdosing lithium has been used to modify the pathological characteristics of the disease, with effects in both experimental and clinical conditions. The present work aimed to analyze the effects of this treatment on spatial memory, anxiety, and molecular mechanisms related to long-term memory formation during the aging process of a mouse model of accelerated aging (SAMP-8). Female SAMP-8 showed learning and memory impairments together with disruption of memory mechanisms, neuronal loss, and increased density of senile plaques compared to their natural control strain, the senescence-accelerated mouse resistant (SAMR-1). Chronic treatment with lithium promoted memory maintenance, reduction in anxiety, and maintenance of proteins related to memory formation and neuronal density. The density of senile plaques was also reduced. An increase in the density of gamma-aminobutyric acid A (GABAA) and α7 nicotinic cholinergic receptors was also observed and related to neuroprotection and anxiety reduction. In addition, this microdose of lithium inhibited the activation of glycogen synthase kinase-3beta (GSK-3β), the classical mechanism of lithium cell effects, which could contribute to the preservation of the memory mechanism and reduction in senile plaque formation. This work shows that lithium effects in neuroprotection along the aging process are not related to a unique cellular mechanism but produce multiple effects that slowly protect the brain along the aging process.
    MeSH term(s) Mice ; Female ; Animals ; Lithium/pharmacology ; Lithium/therapeutic use ; Plaque, Amyloid/pathology ; Glycogen Synthase Kinase 3 beta ; Alzheimer Disease/pathology ; Aging/metabolism ; Disease Models, Animal ; Phenylmercury Compounds
    Chemical Substances Lithium (9FN79X2M3F) ; 4-(4-sulfophenylazo)-2-mercuriphenol (69630-03-1) ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; Phenylmercury Compounds
    Language English
    Publishing date 2024-04-04
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0299534
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Combined Neuroprotective Strategies Blocked Neurodegeneration and Improved Brain Function in Senescence-Accelerated Mice.

    Malerba, Helena Nascimento / Pereira, Arthur Antonio Ruiz / Pierrobon, Marcela Favoretto / Abrao, Guilherme Souza / Toricelli, Mariana / Akamine, Eliana Hiromi / Buck, Hudson Sousa / Viel, Tania Araujo

    Frontiers in aging neuroscience

    2021  Volume 13, Page(s) 681498

    Abstract: Increase in the quality of life, combined with drug strategies, has been studied as possibilities for improving memory and delaying the onset of neurodegenerative diseases. A previous study published by the group of the authors has shown that microdose ... ...

    Abstract Increase in the quality of life, combined with drug strategies, has been studied as possibilities for improving memory and delaying the onset of neurodegenerative diseases. A previous study published by the group of the authors has shown that microdose lithium and enriched environment can improve memory in both mice and humans. To elucidate this relationship better, this study aimed to evaluate whether the chronic combination of these two strategies could increase healthy aging in Senescence Accelerated Mouse-Prone 8 (SAMP8). Animals were submitted to either one or both of these strategies until the age of 10 months when they were anesthetized and killed and their hippocampus was extracted. The untreated SAMP-8 group exhibited worse memory and reduced neuronal density with greater neurodegeneration and increased amyloid-β plaque density compared with the control group. Moreover, significant alterations in proteins related to long-term potentiation, such as, synaptophysin and brain-derived neurotrophic factor (BDNF), were observed in this group. The strategies used in the study maintained long-term memory, reduced anxiety, and increased neuroprotection. Both strategies were efficient in reducing neurodegeneration and increasing parameters related to memory maintenance. In many experiments, the combination of the two strategies was more effective in improving healthy aging. This study sheds light on the combination of strategies that choose to improve the quality of life and drugs with low side effects. Moreover, it opens perspectives for a new field of study for healthy aging.
    Language English
    Publishing date 2021-08-23
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2558898-9
    ISSN 1663-4365
    ISSN 1663-4365
    DOI 10.3389/fnagi.2021.681498
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Mechanisms of neuroplasticity and brain degeneration: strategies for protection during the aging process.

    Toricelli, Mariana / Pereira, Arthur Antonio Ruiz / Souza Abrao, Guilherme / Malerba, Helena Nascimento / Maia, Julia / Buck, Hudson Sousa / Viel, Tania Araujo

    Neural regeneration research

    2020  Volume 16, Issue 1, Page(s) 58–67

    Abstract: Aging is a dynamic and progressive process that begins at conception and continues until death. This process leads to a decrease in homeostasis and morphological, biochemical and psychological changes, increasing the individual's vulnerability to various ...

    Abstract Aging is a dynamic and progressive process that begins at conception and continues until death. This process leads to a decrease in homeostasis and morphological, biochemical and psychological changes, increasing the individual's vulnerability to various diseases. The growth in the number of aging populations has increased the prevalence of chronic degenerative diseases, impairment of the central nervous system and dementias, such as Alzheimer's disease, whose main risk factor is age, leading to an increase of the number of individuals who need daily support for life activities. Some theories about aging suggest it is caused by an increase of cellular senescence and reactive oxygen species, which leads to inflammation, oxidation, cell membrane damage and consequently neuronal death. Also, mitochondrial mutations, which are generated throughout the aging process, can lead to changes in energy production, deficiencies in electron transport and apoptosis induction that can result in decreased function. Additionally, increasing cellular senescence and the release of proinflammatory cytokines can cause irreversible damage to neuronal cells. Recent reports point to the importance of changing lifestyle by increasing physical exercise, improving nutrition and environmental enrichment to activate neuroprotective defense mechanisms. Therefore, this review aims to address the latest information about the different mechanisms related to neuroplasticity and neuronal death and to provide strategies that can improve neuroprotection and decrease the neurodegeneration caused by aging and environmental stressors.
    Language English
    Publishing date 2020-08-11
    Publishing country India
    Document type Journal Article
    ZDB-ID 2388460-5
    ISSN 1876-7958 ; 1673-5374
    ISSN (online) 1876-7958
    ISSN 1673-5374
    DOI 10.4103/1673-5374.286952
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: α7 nicotinic ACh receptors are necessary for memory recovery and neuroprotection promoted by attention training in amyloid-β-infused mice.

    Telles-Longui, Milena / Mourelle, Danilo / Schöwe, Natalia Mendes / Cipolli, Gabriela Cabett / Malerba, Helena Nascimento / Buck, Hudson Sousa / Viel, Tania Araujo

    British journal of pharmacology

    2019  Volume 176, Issue 17, Page(s) 3193–3205

    Abstract: Background and purpose: Attention training reverses the neurodegeneration and memory loss promoted by infusion of amyloid-β (Aβ) peptide in rats and increases the density of α7 nicotinic ACh receptors (α7nAChRs) in brain areas related to memory. Hence, ... ...

    Abstract Background and purpose: Attention training reverses the neurodegeneration and memory loss promoted by infusion of amyloid-β (Aβ) peptide in rats and increases the density of α7 nicotinic ACh receptors (α7nAChRs) in brain areas related to memory. Hence, we aimed to assess the role of α7nAChRs in the memory recovery promoted by attention training.
    Experimental approach: C57Bl/6 mice were chronically infused with Aβ, Aβ plus the α7 antagonist methyllycaconitine (MLA), or MLA alone. Control animals were infused with vehicle. Animals were subjected weekly to the active avoidance shuttle box for 4 weeks (attention training). The brain and serum were collected for biochemical and histological analysis.
    Key results: Aβ caused cognitive impairment, which was reversed by the weekly training, whereas Aβ + MLA also promoted memory loss but with no reversal with weekly training. MLA alone also promoted memory loss but with only partial reversal with the training. Animals infused with Aβ alone showed senile plaques in hippocampus, no change in BDNF levels in cortex, hippocampus, and serum, but increased AChE activity in cortex and hippocampus. Co-treatment with MLA increased AChE activity and senile plaque deposition in hippocampus as well as reducing BDNF in hippocampus and serum, suggesting a lack of α7nAChR function leads to a loss of neuroprotection mechanisms.
    Conclusions and implications: The α7nAChR has a determinant role in memory recovery and brain resilience in the presence of neurodegeneration promoted by Aβ peptide. These data support further studies concerning these receptors as pharmacological targets for future therapies.
    MeSH term(s) Amyloid beta-Peptides/metabolism ; Animals ; Male ; Memory ; Mice ; Mice, Inbred C57BL ; Neuroprotection ; alpha7 Nicotinic Acetylcholine Receptor/metabolism
    Chemical Substances Amyloid beta-Peptides ; alpha7 Nicotinic Acetylcholine Receptor
    Language English
    Publishing date 2019-07-14
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80081-8
    ISSN 1476-5381 ; 0007-1188
    ISSN (online) 1476-5381
    ISSN 0007-1188
    DOI 10.1111/bph.14744
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Kinin B2 Receptor Activation Prevents the Evolution of Alzheimer's Disease Pathological Characteristics in a Transgenic Mouse Model.

    Nunes, Marielza Andrade / Toricelli, Mariana / Schöwe, Natalia Mendes / Malerba, Helena Nascimento / Dong-Creste, Karis Ester / Farah, Daniela Moura Azevedo Tuma / De Angelis, Katia / Irigoyen, Maria Claudia / Gobeil, Fernand / Araujo Viel, Tânia / Buck, Hudson Sousa

    Pharmaceuticals (Basel, Switzerland)

    2020  Volume 13, Issue 10

    Abstract: Background: Alzheimer's disease is mainly characterized by remarkable neurodegeneration in brain areas related to memory formation. This progressive neurodegeneration causes cognitive impairment, changes in behavior, functional disability, and even ... ...

    Abstract Background: Alzheimer's disease is mainly characterized by remarkable neurodegeneration in brain areas related to memory formation. This progressive neurodegeneration causes cognitive impairment, changes in behavior, functional disability, and even death. Our group has demonstrated changes in the kallikrein-kinin system (KKS) in Alzheimer's disease (AD) experimental models, but there is a lack of evidence about the role of the KKS in Alzheimer's disease.
    Aim: In order to answer this question, we evaluated the potential of the kinin B2 receptors (BKB2R) to modify AD characteristics, particularly memory impairment, neurodegeneration, and Aβ peptide deposition.
    Methods: To assess the effects of B2, we used transgenic Alzheimer's disease mice treated with B2 receptor (B2R) agonists and antagonists, and performed behavioral and biochemical tests. In addition, we performed organotypic hippocampal culture of wild-type (WT) and transgenic (TG) animals, where the density of cytokines, neurotrophin BDNF, activated astrocyte marker S100B, and cell death were analyzed after treatments.
    Results: Treatment with the B2R agonist preserved the spatial memory of transgenic mice and decreased amyloid plaque deposition. In organotypic hippocampal culture, treatment with B2R agonist decreased cell death, neuroinflammation, and S100B levels, and increased BDNF release.
    Conclusions: Our results indicate that the kallikrein-kinin system plays a beneficial role in Alzheimer's disease through B2R activation. The use of B2R agonists could, therefore, be a possible therapeutic option for patients diagnosed with Alzheimer's disease.
    Language English
    Publishing date 2020-10-01
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2193542-7
    ISSN 1424-8247
    ISSN 1424-8247
    DOI 10.3390/ph13100288
    Database MEDical Literature Analysis and Retrieval System OnLINE

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