Oral fluoxetine in the management of amblyopic patients aged between 10 and 40 years old: a randomized clinical trial.

Objective: The objective of this study is to assess the efficacy of oral fluoxetine therapy in improving the visual function of amblyopic patients aged between 10 and 40 years old.

Methods: In this double-blinded, randomized, controlled trial (IRCT2016052428046N1; registered retrospectively), 40 eligible participants with anisometropic or mixed amblyopia were randomly assigned to either fluoxetine or placebo groups. Participants with anisometropia and logMAR best spectacle-corrected visual acuity (BSCVA) worse than 0.

Insulin potentiates the therapeutic effect of memantine against central STZ-induced spatial learning and memory deficit.

Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder. Memantine has been approved for moderate to severe AD, but evidence indicates that it does not modify disease progression. Recently insulin has been found to exert some beneficial effects on cognition.

The Interplay of Akt and ERK in Aβ Toxicity and Insulin-Mediated Protection in Primary Hippocampal Cell Culture.

It is not known if insulin prevents Aβ-induced cell death, MAPK, and Akt activity in isolated hippocampal cell culture. This study was aimed to explore the effect of insulin on Aβ-induced cell death and ERK and Akt signaling alteration in isolated hippocampal cell culture. Additionally, it was desirable to assess if there is any interaction between these two pathways.

Insulin protects against Aβ-induced spatial memory impairment, hippocampal apoptosis and MAPKs signaling disruption.

Alzheimer disease (AD) is a progressive neurodegenerative disease characterized by extracellular deposits of beta amyloid (Aβ) and neuronal loss particularly in the hippocampus. Accumulating evidences have implied that insulin signaling impairment plays a key role in the pathology of AD; as much as it is considered as type 3 Diabetes. MAPKs are a group of signaling molecules which are involved in pathobiology of AD.

The role of nitric oxide in spatial memory stages, hippocampal ERK and CaMKII phosphorylation.

Nitric oxide (NO) is an important intercellular messenger in the control of physiologic functions. It is synthesized by 3 different nitric oxide synthase enzymes (NOS). Uses of non-selective NOS inhibitor (L-NAME) have shown that NO is involved in neuronal plasticity and memory.

Perindopril may improve the hippocampal reduced glutathione content in rats.

Purpose: Oxidative stress and renin- angiotensin system are both involved in the pathophysiology of most of the systemic and central disorders as well as in aging. Angiotensin converting enzyme (ACE) inhibitors, well known for their cardiovascular beneficial effects, have also shown antioxidant properties in pathologic conditions. This study aimed to evaluate the central effect of ACE inhibitors on oxidative status under no pathologic condition.

Repeated intra-hippocampal injection of beta-amyloid 25–35 induces a reproducible impairment of learning and memory: considering caspase-3 and MAPKs activity.

Alzheimer disease (AD) is characterized by accumulation of beta amyloid (Aβ) and neuronal loss, particularly in the hippocampus. Direct central administration of this peptide was suggested as a route to create an animal model of AD. Although there are some studies indicating that a single dose of Aβ induces AD-like learning and memory impairment, this model is not usually reproducible especially in rat.

Agmatine protects against scopolamine-induced water maze performance impairment and hippocampal ERK and Akt inactivation.

Cholinergic brain activity plays a significant role in memory. Scopolamine a muscarinic cholinergic antagonist is known to induce impairment in Morris water maze performance, the task which is mainly dependent on the hippocampus. It is suggested that hippocampal ERK and Akt activation play roles in synaptic plasticity and some types of learning and memory.

The effect of sub-anesthetic and anesthetic ketamine on water maze memory acquisition, consolidation and retrieval.

Ketamine, a non-selective inhibitor of NMDA (N-methyl-D-aspartate) channels is used in anesthetic or sub-anesthetic doses to induce analgesia, amnesia, to suppress fear, anxiety and depression. Although the ketamine's effect on memory acquisition is known, its effects on other aspects of memory are controversial. Morris water maze is a task which assesses spatial learning and memory.

The relation between pregnancy and stress in rats: considering corticosterone level, hippocampal caspase-3 and MAPK activation.

Objectives: There are some evidences indicating that stress can affect hippocampal survival and function. During pregnancy mother is exposed to more stress and anxiety; also adrenal gland response to ACTH and glucocorticoid secretion is increased. Hence this study was done to assess the effect of restraint stress on corticosterone level, hippocampal caspase-3 and MAPK activation during pregnancy.

Agmatine prevents LPS-induced spatial memory impairment and hippocampal apoptosis.

Neuroinflammation is associated with a number of neurodegenerative diseases. It is known that lipopolysaccharide (LPS) treatment induces neuroinflammation and memory deterioration. Agmatine, the metabolite of arginine by arginine decarboxylase, is suggested to be a neuroprotective agent.

Different fibrillar Abeta 1-42 concentrations induce adult hippocampal neurons to reenter various phases of the cell cycle.

In Alzheimer's disease (AD) cell cycle reentry precedes neuronal death, which could be induced by many cytotoxic factors. It is believed that beta amyloid (Abeta), the major component of extracellular plaques in AD, is potent in inducing neurons to reenter cell cycle. In AD brains, neurons expressing cell cycle markers are reported in many brain regions without any plaque formation, although very low levels of Abeta may still be detected.

Culturing adult rat hippocampal neurons with long-interval changing media.

Background: Primary cultures of embryonic neurons have been used to introduce a model of neurons in physiological and pathological conditions. However, age-related cellular events limit this method as an optimal model in adult neurodegenerative diseases studies. Besides, short-interval changing media in previous cultures decreases the effectiveness of this model.

Fibrillar beta-amyloid (Abeta) (1-42) elevates extracellular Abeta in cultured hippocampal neurons of adult rats.

Alzheimer's disease (AD) is a chronic disorder with progressive neurodegeneration associated with aging and is characterized by fibrillar beta-amyloid (Abeta) deposits in the brain. Although the increased production of Abeta seems to play a noticeable role in AD pathogenesis and its progression, all the mechanisms which are involved in this extracellular Abeta elevation are not known completely. In the present study, we used adult hippocampal neuronal culture as an in vitro model which is favorable for adult neurodegenerative diseases' studies.