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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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Article ; Online: Microdose Lithium Treatment Reduced Inflammatory Factors and Neurodegeneration in Organotypic Hippocampal Culture of Old SAMP-8 Mice.

Toricelli, Mariana / Evangelista, Sebastiana Ribeiro / Buck, Hudson Sousa / Viel, Tania Araujo

Cellular and molecular neurobiology

2020 Volume 41, Issue 7, Page(s) 1509–1520

Abstract: It was already shown that microdoses of lithium carbonate ( ... ...

Abstract	It was already shown that microdoses of lithium carbonate (Li
MeSH term(s)	Alzheimer Disease/drug therapy ; Alzheimer Disease/metabolism ; Animals ; Cell Death/drug effects ; Disease Models, Animal ; Hippocampus/drug effects ; Hippocampus/metabolism ; Lithium/pharmacology ; Mice, Transgenic ; Neurons/drug effects ; Neurons/metabolism ; Neuroprotective Agents/pharmacology ; Phenylmercury Compounds/pharmacology
Chemical Substances	Neuroprotective Agents ; Phenylmercury Compounds ; 4-(4-sulfophenylazo)-2-mercuriphenol (69630-03-1) ; Lithium (9FN79X2M3F)
Language	English
Publishing date	2020-07-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	283404-2
ISSN	1573-6830 ; 0272-4340
ISSN (online)	1573-6830
ISSN	0272-4340
DOI	10.1007/s10571-020-00916-0
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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
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Article: Neuroprotective Effects of Kinin B2 Receptor in Organotypic Hippocampal Cultures of Middle-Aged Mice.

Toricelli, Mariana / Evangelista, Sebastiana Ribeiro / Oliveira, Larissa Rolim / Viel, Tania Araujo / Buck, Hudson Sousa

Frontiers in aging neuroscience

2019 Volume 11, Page(s) 168

Abstract: Aging is a multifactorial phenomenon that results in several changes at cellular and molecular levels and is considered the main risk factor for some neurodegenerative diseases. Several evidence show the participation of the kallikrein-kinin system (KKS) ...

Abstract	Aging is a multifactorial phenomenon that results in several changes at cellular and molecular levels and is considered the main risk factor for some neurodegenerative diseases. Several evidence show the participation of the kallikrein-kinin system (KKS) in neurodegeneration and this system has been associated with inflammation and immunogenic responses in the central and peripheral systems by the activation of the B1 and B2 receptors. Previous work by our group showed that bradykinin (BK) and the B2 receptor played a possible role in neuroprotection. Therefore, the objective of this study was to evaluate the participation of B2 receptors in cell viability, neuroinflammatory response and neuroplasticity in organotypic hippocampal cultures (OHCs) of 6- and 12-month-old mice. It was observed that activation of the B2 receptor by bradykinin decreased the inflammatory response and increased plasticity in 12-month-old slices. Conversely, there was an increase in the inflammatory response and a decrease in neural plasticity in the 6-month-old slices. In both ages, an increase in cell viability was observed. This data suggests that the function of the kinin B2 receptor in the hippocampus is modulated by age, providing neuroprotective action in old age.
Language	English
Publishing date	2019-07-12
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2019.00168
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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
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Article: Enriched Environment Significantly Reduced Senile Plaques in a Transgenic Mice Model of Alzheimer's Disease, Improving Memory.

Balthazar, Janaina / Schöwe, Natalia Mendes / Cipolli, Gabriela Cabett / Buck, Hudson Sousa / Viel, Tania Araujo

Frontiers in aging neuroscience

2018 Volume 10, Page(s) 288

Abstract: Alzheimer's disease (AD) is associated with a progressive dementia, and there is good evidence that it is more pronounced in individuals that have fewer stimuli during their lives. Environmental stimulation promotes morphological and functional changes ... ...

Abstract	Alzheimer's disease (AD) is associated with a progressive dementia, and there is good evidence that it is more pronounced in individuals that have fewer stimuli during their lives. Environmental stimulation promotes morphological and functional changes in the brain, leading to amplification of cognitive functions, and has been described in humans and animals. In this study, we evaluated the effects of enriched environment (EE) stimulation on spatial memory and senile plaque formation in transgenic mice PDGFB-APPSwInd (TG) that overexpress the human amyloid precursor protein, normally resulting in an increased density of senile plaques. We compared this group of EE stimulated transgenic mice (TG-EE) with an EE stimulated control group of age-matched C57Bl/6 wild type animals (WT-EE). Both groups were exposed to EE stimulation between the ages of 8 and 12 months. As controls of the experiment, there were a group of TG mice not exposed to EE (TG-Ctrl) and a group of WT mice not exposed to EE (WT-Ctrl). The TG-EE group presented improved spatial memory when compared to the TG-Ctrl animals. In addition, the TG-EE group showed a 69.2% reduction in the total density of senile plaques in the hippocampus when compared to the TG-Ctrl group. In this group, the concentration of senile plaques was greater in the dorsal part of the hippocampus, which is linked to spatial localization, and the reduction of this density after the submission to EE was as high as 85.1%. EE stimulation had no effect on the density of amyloid-β (Aβ) oligomers. However, amyloid scavenger receptor class B member 1 (SR-B1) density was significantly decreased in the TG-Ctrl mice, but not in the TG-EE mice, suggesting that cognitive stimulation had an effect on the formation of a cognitive reserve that could prevent the accumulation of senile plaques. It is suggested that the stimulation of old mice by EE for 4 months led to the formation of brain resilience that protected the brain from the deposition of senile plaques, one of the hallmarks of AD, leading to improvement in spatial memory.
Language	English
Publishing date	2018-09-26
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2018.00288
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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
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Article: Dataset for the role of sustained attention in memory formation of transgenic mice for Alzheimer׳s disease

Schöwe, Natalia Mendes / de Oliveira, Eduardo Moreira / Buck, Hudson Sousa / Viel, Tania Araujo

Data in Brief. 2016 Mar., v. 6

2016

Abstract: Weekly submission of rats to active avoidance apparatus can be considered a neurostimulation strategy, once it can improve memory and can increase the density of receptors from different neurotransmitter systems in brain areas related to memory. These ... ...

Abstract	Weekly submission of rats to active avoidance apparatus can be considered a neurostimulation strategy, once it can improve memory and can increase the density of receptors from different neurotransmitter systems in brain areas related to memory. These benefits were observed in rats chronically infused with amyloid-β peptide. In the present work it is presented that the same benefit for memory was observed in five months old transgenic mice for Alzheimer’s disease (TG-PDGFB-APPSw,Iₙd). However, at this age, no change in density of nicotinic receptors was observed.
Keywords	brain ; data collection ; memory ; neurotransmitters ; peptides
Language	English
Dates of publication	2016-03
Size	p. 763-768.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	2786545-9
ISSN	2352-3409
ISSN	2352-3409
DOI	10.1016/j.dib.2016.01.015
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Microdose lithium treatment stabilized cognitive impairment in patients with Alzheimer's disease.

Nunes, Marielza Andrade / Viel, Tania Araujo / Buck, Hudson Sousa

Current Alzheimer research

2012 Volume 10, Issue 1, Page(s) 104–107

Abstract: A lower incidence of dementia in bipolar patients treated with lithium has been described. This metal inhibits the phosphorylation of glycogen-synthase-kinase 3-α and β, which are related to amyloid precursor protein processing and tau ... ...

Abstract	A lower incidence of dementia in bipolar patients treated with lithium has been described. This metal inhibits the phosphorylation of glycogen-synthase-kinase 3-α and β, which are related to amyloid precursor protein processing and tau hyperphosphorylation in pathological conditions, respectively. Following the same rationale, a group just found that lithium has disease-modifying properties in amnestic mild cognitive impairment with potential clinical implications for the prevention of Alzheimer's Disease (AD) when a dose ranging from 150 to 600 mg is used. As lithium is highly toxic in regular doses, our group evaluated the effect of a microdose of 300 μg, administered once daily on AD patients for 15 months. In the evaluation phase, the treated group showed no decreased performance in the mini-mental state examination test, in opposition to the lower scores observed for the control group during the treatment, with significant differences starting three months after the beginning of the treatment, and increasing progressively. This data suggests the efficacy of a microdose lithium treatment in preventing cognitive loss, reinforcing its therapeutic potential to treat AD using very low doses.
MeSH term(s)	Adjuvants, Immunologic/therapeutic use ; Aged ; Alzheimer Disease/complications ; Analysis of Variance ; Cognition Disorders/drug therapy ; Cognition Disorders/etiology ; Double-Blind Method ; Female ; Humans ; Lithium Chloride/therapeutic use ; Male ; Psychiatric Status Rating Scales
Chemical Substances	Adjuvants, Immunologic ; Lithium Chloride (G4962QA067)
Language	English
Publishing date	2012-02-21
Publishing country	United Arab Emirates
Document type	Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
ZDB-ID	2205170-3
ISSN	1875-5828 ; 1567-2050
ISSN (online)	1875-5828
ISSN	1567-2050
DOI	10.2174/1567205011310010014
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Article: Dataset for the role of sustained attention in memory formation of transgenic mice for Alzheimer׳s disease.

Schöwe, Natalia Mendes / de Oliveira, Eduardo Moreira / Buck, Hudson Sousa / Viel, Tania Araujo

Data in brief

2016 Volume 6, Page(s) 763–768

Abstract	Weekly submission of rats to active avoidance apparatus can be considered a neurostimulation strategy, once it can improve memory and can increase the density of receptors from different neurotransmitter systems in brain areas related to memory. These benefits were observed in rats chronically infused with amyloid-β peptide. In the present work it is presented that the same benefit for memory was observed in five months old transgenic mice for Alzheimer's disease (TG-PDGFB-APPSw,Ind). However, at this age, no change in density of nicotinic receptors was observed.
Language	English
Publishing date	2016-01-16
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2786545-9
ISSN	2352-3409
ISSN	2352-3409
DOI	10.1016/j.dib.2016.01.015
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