Publications by authors named "Ana Flávia Fernandes Ferreira"

4 Publications

  • Page 1 of 1

Association between thyroid function and Alzheimer's disease: A systematic review.

Metab Brain Dis 2021 Jun 19. Epub 2021 Jun 19.

Laboratory of Neuronal Communication, Departamento de Fisiologia e Biofisica, Universidade de Sao Paulo, Av. Professor Lineu Prestes, 1524 - Cidade Universitária, São Paulo, SP, Brasil, 05508900.

Alterations in metabolic parameters have been associated with an increased risk of dementia, among which thyroid function has gained great importance in Alzheimer's disease (AD) pathology in recent years. However, it remains unclear whether thyroid dysfunctions could influence and contribute to the beginning and/or progression of AD or if it results from AD. This systematic review was conducted to examine the association between thyroid hormone (TH) levels and AD. Medline, ISI Web of Science, EMBASE, Cochrane library, Scopus, Scielo, and LILACS were searched, from January 2010 to March 2020. A total of 17 articles were selected. The studies reported alterations in TH and circadian rhythm in AD patients. Behavior, cognition, cerebral blood flow, and glucose consumption were correlated with TH deficits in AD patients. Whether thyroid dysfunctions and AD have a cause-effect relationship was inconclusive, however, the literature was able to provide enough data to corroborate a relationship between TH and AD. Although further studies are needed in this field, the current systematic review provides information that could help future investigations.
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June 2021

Maternal Immune Activation with H1N1 or Toxoplasma gondii Antigens Induces Behavioral Impairments Associated with Mood Disorders in Rodents.

Neuropsychobiology 2021 16;80(3):234-241. Epub 2020 Oct 16.

Physiology Department, Institute of Biomedical Sciences, Federal University of Uberlândia, Uberlândia, Brazil.

Introduction: Epidemiological studies revealed that maternal exposure to influenza A (H1N1) and Toxoplasma gondii (T. gondii) infection during pregnancy may increase the risk for mood disorders of the offspring. However, the impact of maternal infections in different stages of neural development and the nature of antigens remain to be elucidated.

Objective: This study investigated behavioral impairments induced by maternal immune activation (MIA) due to H1N1 or T. gondii infection during preborn neurodevelopment.

Methods: Maternal infection with influenza or toxoplasma was mimicked by administration of influenza vaccine antigens or suspension of soluble T. gondii antigen (STAg) in pregnant Balb/c mice at E6 or E16. Adult male offspring were evaluated for anxiety-like and depressive-like behavior in elevated plus maze (EPM) and forced swimming test (FST).

Results: In FST, immobility time at E6 and E16 increased when the mothers were treated with both antigen solutions. There was increased immobility in the pups whose mothers were treated with STAg at E16. MIA with influenza antigens reduced the exploration of the open arms of EPM for the pups whose progenitors received treatment at E6 and E16. The animals at E6 exhibited a greater number of stretch-attend postures compared with the saline group. STAg at E6 reduced the time of exploration in the open arms and increased the number of stretch-attend postures compared with the saline group.

Conclusion: These results suggest that immunological responses to H1N1 or T. gondii during pregnancy may impact differently the susceptibility of adult offspring to mood disorder.
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October 2020

Physical exercise protects against mitochondria alterations in the 6-hidroxydopamine rat model of Parkinson's disease.

Behav Brain Res 2020 06 18;387:112607. Epub 2020 Mar 18.

Laboratory of Cellular Neurobiology, Department of Physiology and Biophysics, Biomedical Science Institute, University of São Paulo, São Paulo, SP, Brazil. Electronic address:

Parkinson's disease (PD) is typicaly caractherized by loss of dopaminergic neurons, as well as the presence of mitochondrial impairments. Although physical exercise is known to promote many beneficial effects in healthy subjects, such as enhancing mitocondrial biogenesis and function, it is not clear if these effects are evident after exercise in individuals with PD. The aim of this study was to investigate the effects of two different protocol durations on motor behavior (aphomorphine and gait tests), mitochondrial biogenesis signaling (PGC-1α, NRF-1 and TFAM), structure (oxidative phosphorylation system protein levels) and respiratory chain activity (complex I) in a unilateral PD rat model. For this, male Wistar rats were injected with 6-hydroxydopamine unilaterally into the striatum and submitted to an intermitent moderate treadmill exercise for one or four weeks. In the gait test, only stride width data revealed an improvement after one week of exercise. On the other hand, after 4 weeks of the exercise protocol all gait parameters analyzed and the aphomorphine test demonstrated a recovery. Analysis of protein revealed that one week of exercise was able to prevent PGC-1α and NRF-1 expression decrease in PD animals. In addition, after four weeks of physical exercise, besides PGC-1α and NRF-1, reduction in TFAM and complex I protein levels and increased complex I activity were also prevented in PD animals. Thus, our results suggest a neuroprotective and progressive effect of intermittent treadmill exercise, which could be related to its benefits on mitochondrial biogenesis signaling and respiratory chain modulation of the dopaminergic system in PD.
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June 2020

Impairment of PGC-1α-mediated mitochondrial biogenesis precedes mitochondrial dysfunction and Alzheimer's pathology in the 3xTg mouse model of Alzheimer's disease.

Exp Gerontol 2020 05 19;133:110882. Epub 2020 Feb 19.

Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil. Electronic address:

Impairment of mitochondrial biogenesis and mitochondrial dysfunction is a prominent feature of Alzheimer's disease (AD). However, the extent to which the impairment of mitochondrial biogenesis influences mitochondrial dysfunction at the onset and during progression of AD is still unclear. Our study demonstrated that the protein expression pattern of the transcription factor pCREB/CREB, together with the protein expression of PGC-1α, NRF1 and TFAM are all significantly reduced in early ages of 3xTg-AD mice. We also found reduced mRNA expression levels of PKAC-α, CREB, PGC-1α, NRF1, NRF2 and TFAM as early as 1 month-of-age, an age at which there was no significant Aβ oligomer deposition, suggesting that mitochondrial biogenesis is likely impaired in ages preceding the development of the AD pathology. In addition, there was a decrease in VDAC2 expression, which is related to mitochondrial content and mitochondrial function, as demonstrated by protein expression of complex IV, as well as complex II + III, and complex IV activities, at later ages in 3xTg-AD mice. These results suggest that the impairment in mitochondrial biogenesis signaling mediated by PGC-1α at early ages of the AD mice model likely resulted in mitochondrial dysfunction and manifestation of the AD pathology at later ages. Taken together, enhancing mitochondrial biogenesis may represent a potential pharmacological approach for the treatment of AD.
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May 2020