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Neuroprotective Effect of Chlorogenic Acid in an Animal Model of Sporadic Alzheimer's Disease Induced by Streptozotocin.
Bezerra, Jéssica Rabelo; de Souza Nascimento, Tyciane; Tavares, Juliete; de Aguiar, Mayara Sandrielly Soares; Maia, Maiara Virgínia Viana; de Andrade, Geanne Matos.
Afiliação
  • Bezerra JR; Department of Physiology and Pharmacology, Faculty of Medicine, Federal University of Ceara, Rua Cel. Nunes de Melo 1127, Porangabussu, Fortaleza, Ceará, 60430-270, Brazil.
  • de Souza Nascimento T; Laboratory of Neuroscience and Behavior, Drug Research and Development Center (NPDM), , Federal University of Ceará, Rua Coronel Nunes de Melo 1127, Porangabussu, Fortaleza, Ceará, 60430-270, Brazil.
  • Tavares J; Department of Clinical Medicine, Faculty of Medicine, Federal University of Ceara, Rua Costa Mendes, Porangabussu, Fortaleza, Ceará, 160860430-140, Brazil.
  • de Aguiar MSS; Laboratory of Neuroscience and Behavior, Drug Research and Development Center (NPDM), , Federal University of Ceará, Rua Coronel Nunes de Melo 1127, Porangabussu, Fortaleza, Ceará, 60430-270, Brazil.
  • Maia MVV; Department of Clinical Medicine, Faculty of Medicine, Federal University of Ceara, Rua Costa Mendes, Porangabussu, Fortaleza, Ceará, 160860430-140, Brazil.
  • de Andrade GM; Laboratory of Neuroscience and Behavior, Drug Research and Development Center (NPDM), , Federal University of Ceará, Rua Coronel Nunes de Melo 1127, Porangabussu, Fortaleza, Ceará, 60430-270, Brazil.
Mol Neurobiol ; 2024 Jun 19.
Article em En | MEDLINE | ID: mdl-38898198
ABSTRACT
Alzheimer's Disease is a degenerative neurological condition which leads to a decline in memory and cognitive function. Chlorogenic Acid (CGA) presents properties including neuroprotective, antioxidant and anti-inflammatory. The aim of this study was to examine the impact of CGA on cognitive impairments, neuroinflammation and neuronal damage in mice submitted to an experimental model of Sporadic Alzheimer Disease (SAD) induced by intracerebroventricular administration of streptozotocin (ICV-STZ). Male Swiss mice received bilateral ICV-STZ injections (3 mg/Kg) on days 1 and 3. The treatment with CGA (5 mg/Kg, orally) or vehicle (water, orally), was initiated and continued for 26 days, starting 2 h after the second induction procedure. At first, there was no change in serum glucose levels after SAD induction. ICV-STZ induces impairments in aversive, recognition, and spatial memory, while CGA treatment significantly alleviated these memory deficits. Furthermore, locomotor activity, working memory, and anxiety-related activities remained unaffected by the treatments. CGA treatment protects against ICV-STZ-induced increase in the nitrite/nitrate and TBARS levels. ICV-STZ induced a reduction in viable cells, depletion of BDNF, and triggered astrogliosis and microgliosis in the cortex and hippocampus. Treatment with CGA preserves viable cell count in the prefrontal cortex, CA1, and CA3 regions of the hippocampus. Additionally, it prevented BDNF depletion in the prefrontal cortex and hippocampus (CA1, CA3, and DG regions), and mitigated astrogliosis and microgliosis in the prefrontal cortex and hippocampus (CA1, CA3, and DG regions). These findings indicate the neuroprotective effects of CGA, underscoring their potential as therapeutic agents or adjuncts in the treatment of SAD.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Mol Neurobiol Assunto da revista: BIOLOGIA MOLECULAR / NEUROLOGIA Ano de publicação: 2024 Tipo de documento: Article País de afiliação: Brasil País de publicação: Estados Unidos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Mol Neurobiol Assunto da revista: BIOLOGIA MOLECULAR / NEUROLOGIA Ano de publicação: 2024 Tipo de documento: Article País de afiliação: Brasil País de publicação: Estados Unidos