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Alzheimer's disease (AD) is a progressive neurodegenerative disease that causes gradual memory loss and cognitive impairment. Intracerebroventricular injections of streptozotocin (ICV-STZ) have been used as an experimental model of sporadic Alzheimer's disease (SAD) because they produce deficits in brain insulin signaling, oxidative stress, neuroinflammation, and neurodegeneration, resulting in cognitive decline and memory impairment. Spirulina platensis (SPI) is a nutraceutical with anti-inflammatory, antioxidant, and neuroprotective properties. The objective of this work was to study the effects of SPI on cognitive deficits and neuronal damage in mice submitted to the experimental model of SAD induced by ICV-STZ. Male Swiss mice (25-35 g) received ICV-STZ (3 mg/Kg) bilaterally on days 1 and 3, SPI (50 and 100 mg/Kg, o.p.) or vehicle (saline) was administered 2 h after the second surgery, and once a day for 16 days. SPI treatment prevented working, episodic, spatial, and aversive memory deficits. Locomotor activity was not altered. ICV-STZ caused an increase in MDA, nitrite, and superoxide anion, while decreasing GSH. SPI treatment protected against GSH increase in the prefrontal cortex and hippocampus, and inhibited AChE activity in the prefrontal cortex. SPI prevented astrogliosis and microgliosis induced by ICV-STZ. These findings highlight the therapeutic potential of SPI for the treatment of SAD, indicating that its neuroprotective action is linked to antioxidant, anti-inflammatory, and AChE inhibitory activity., Competing Interests: Declarations. Ethics committee: All procedures in this study are in accordance with the Guide for the Care and Use of Laboratory Animals of the US Health and Human Services Department and were approved by the ethics committee in animal experimentation of the Federal University of Ceará, under registration number 3598100320. Consent to participate: Not applicable. Competing interests: The authors declare no competing interests., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Ischemic stroke is one of the major causes of human morbidity and mortality. The pathophysiology of ischemic stroke involves complex events, including oxidative stress and inflammation, that lead to neuronal loss and cognitive deficits. Palmatine (PAL) is a naturally occurring (Coptidis rhizome) isoquinoline alkaloid that belongs to the class of protoberberines and has a wide spectrum of pharmacological and biological effects. In the present study, we evaluated the impact of Palmatine on neuronal damage, memory deficits, and inflammatory response in mice submitted to permanent focal cerebral ischemia induced by middle cerebral artery (pMCAO) occlusion. The animals were treated with Palmatine (0.2, 2 and 20 mg/kg/day, orally) or vehicle (3% Tween + saline solution) 2 h after pMCAO once daily for 3 days. Cerebral ischemia was confirmed by evaluating the infarct area (TTC staining) and neurological deficit score 24 h after pMCAO. Treatment with palmatine (2 and 20 mg/kg) reduced infarct size and neurological deficits and prevented working and aversive memory deficits in ischemic mice. Palmatine, at a dose of 2 mg/kg, had a similar effect of reducing neuroinflammation 24 h after cerebral ischemia, decreasing TNF-, iNOS, COX-2, and NF- κB immunoreactivities and preventing the activation of microglia and astrocytes. Moreover, palmatine (2 mg/kg) reduced COX-2, iNOS, and IL-1β immunoreactivity 96 h after pMCAO. The neuroprotective properties of palmatine make it an excellent adjuvant treatment for strokes due to its inhibition of neuroinflammation., Competing Interests: Declaration of Competing Interest The authors report no conflict of interest., (Copyright © 2023 Elsevier B.V. All rights reserved.)