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Curcumin Improves Amyloid β-Peptide (1-42) Induced Spatial Memory Deficits through BDNF-ERK Signaling Pathway.

Zhang L, Fang Y, Xu Y, Lian Y, Xie N, Wu T, Zhang H, Sun L, Zhang R, Wang Z - PLoS ONE (2015)

Bottom Line: Curcumin, the most active component of turmeric, has various beneficial properties, such as antioxidant, anti-inflammatory, and antitumor effects.In addition, the beneficial effect of curcumin is accompanied by increased BDNF levels and elevated levels of phosphorylated ERK in the hippocampus.Furthermore, the cognition enhancement effect of curcumin could be mimicked by the overexpression of BDNF in the hippocampus and blocked by either bilateral hippocampal injections with lentiviruses that express BDNF shRNA or a microinjection of ERK inhibitor.

View Article: PubMed Central - PubMed

Affiliation: Key-Disciplines Laboratory Clinical-Medicine of Henan, Zhengzhou, Henan, PR China; Department of Neurology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, PR China.

ABSTRACT
Curcumin, the most active component of turmeric, has various beneficial properties, such as antioxidant, anti-inflammatory, and antitumor effects. Previous studies have suggested that curcumin reduces the levels of amyloid and oxidized proteins and prevents memory deficits and thus is beneficial to patients with Alzheimer's disease (AD). However, the molecular mechanisms underlying curcumin's effect on cognitive functions are not well-understood. In the present study, we examined the working memory and spatial reference memory in rats that received a ventricular injection of amyloid-β1-42 (Aβ1-42), representing a rodent model of Alzheimer's disease (AD). The rats treated with Aβ1-42 exhibited obvious cognitive deficits in behavioral tasks. Chronic (seven consecutive days, once per day) but not acute (once a day) curcumin treatments (50, 100, and 200 mg/kg) improved the cognitive functions in a dose-dependent manner. In addition, the beneficial effect of curcumin is accompanied by increased BDNF levels and elevated levels of phosphorylated ERK in the hippocampus. Furthermore, the cognition enhancement effect of curcumin could be mimicked by the overexpression of BDNF in the hippocampus and blocked by either bilateral hippocampal injections with lentiviruses that express BDNF shRNA or a microinjection of ERK inhibitor. These findings suggest that chronic curcumin ameliorates AD-related cognitive deficits and that upregulated BDNF-ERK signaling in the hippocampus may underlie the cognitive improvement produced by curcumin.

No MeSH data available.


Related in: MedlinePlus

The experimental protocol of the Morris water maze for acute or repeated curcumin treatment.
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pone.0131525.g001: The experimental protocol of the Morris water maze for acute or repeated curcumin treatment.

Mentions: To assess spatial reference learning and memory, a separate cohort of rats from both the acute and repeated treatment groups were tested in the Morris water maze. The experimental apparatus (RWD Life Science, Shenzhen, China) consisted of a circular water pool (diameter 150 cm; height 60 cm; containing water at 24±2°C) divided into four equally spaced quadrants. The pool was placed in a test room containing various prominent visual cues. A translucent 10 × 10 cm platform submerged 1 cm below the water surface was hidden at the center of quadrant II during the training period and was then removed at the time of the probe task. Memory training was performed 5 days after Aβ1–42 injection. The training was conducted twice per day for five consecutive days before the probe task. Each rat was allowed to swim until it found the platform or until 120 s elapsed. The rat was then left on the platform for 10 s. During the spatial probe task, the platform was removed from the pool, and the rats were allowed to swim for 120 s. The swim escape latency, average swim speed, time spent in the target quadrant, and number of times the animal crossed the previous location of the platform were recorded by a video tracking system (SMART, Panlab SL, Barcelona, Spain). The experimental procedures for acute and chronic curcumin treatment are outlined in Fig 1A.


Curcumin Improves Amyloid β-Peptide (1-42) Induced Spatial Memory Deficits through BDNF-ERK Signaling Pathway.

Zhang L, Fang Y, Xu Y, Lian Y, Xie N, Wu T, Zhang H, Sun L, Zhang R, Wang Z - PLoS ONE (2015)

The experimental protocol of the Morris water maze for acute or repeated curcumin treatment.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4482657&req=5

pone.0131525.g001: The experimental protocol of the Morris water maze for acute or repeated curcumin treatment.
Mentions: To assess spatial reference learning and memory, a separate cohort of rats from both the acute and repeated treatment groups were tested in the Morris water maze. The experimental apparatus (RWD Life Science, Shenzhen, China) consisted of a circular water pool (diameter 150 cm; height 60 cm; containing water at 24±2°C) divided into four equally spaced quadrants. The pool was placed in a test room containing various prominent visual cues. A translucent 10 × 10 cm platform submerged 1 cm below the water surface was hidden at the center of quadrant II during the training period and was then removed at the time of the probe task. Memory training was performed 5 days after Aβ1–42 injection. The training was conducted twice per day for five consecutive days before the probe task. Each rat was allowed to swim until it found the platform or until 120 s elapsed. The rat was then left on the platform for 10 s. During the spatial probe task, the platform was removed from the pool, and the rats were allowed to swim for 120 s. The swim escape latency, average swim speed, time spent in the target quadrant, and number of times the animal crossed the previous location of the platform were recorded by a video tracking system (SMART, Panlab SL, Barcelona, Spain). The experimental procedures for acute and chronic curcumin treatment are outlined in Fig 1A.

Bottom Line: Curcumin, the most active component of turmeric, has various beneficial properties, such as antioxidant, anti-inflammatory, and antitumor effects.In addition, the beneficial effect of curcumin is accompanied by increased BDNF levels and elevated levels of phosphorylated ERK in the hippocampus.Furthermore, the cognition enhancement effect of curcumin could be mimicked by the overexpression of BDNF in the hippocampus and blocked by either bilateral hippocampal injections with lentiviruses that express BDNF shRNA or a microinjection of ERK inhibitor.

View Article: PubMed Central - PubMed

Affiliation: Key-Disciplines Laboratory Clinical-Medicine of Henan, Zhengzhou, Henan, PR China; Department of Neurology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, PR China.

ABSTRACT
Curcumin, the most active component of turmeric, has various beneficial properties, such as antioxidant, anti-inflammatory, and antitumor effects. Previous studies have suggested that curcumin reduces the levels of amyloid and oxidized proteins and prevents memory deficits and thus is beneficial to patients with Alzheimer's disease (AD). However, the molecular mechanisms underlying curcumin's effect on cognitive functions are not well-understood. In the present study, we examined the working memory and spatial reference memory in rats that received a ventricular injection of amyloid-β1-42 (Aβ1-42), representing a rodent model of Alzheimer's disease (AD). The rats treated with Aβ1-42 exhibited obvious cognitive deficits in behavioral tasks. Chronic (seven consecutive days, once per day) but not acute (once a day) curcumin treatments (50, 100, and 200 mg/kg) improved the cognitive functions in a dose-dependent manner. In addition, the beneficial effect of curcumin is accompanied by increased BDNF levels and elevated levels of phosphorylated ERK in the hippocampus. Furthermore, the cognition enhancement effect of curcumin could be mimicked by the overexpression of BDNF in the hippocampus and blocked by either bilateral hippocampal injections with lentiviruses that express BDNF shRNA or a microinjection of ERK inhibitor. These findings suggest that chronic curcumin ameliorates AD-related cognitive deficits and that upregulated BDNF-ERK signaling in the hippocampus may underlie the cognitive improvement produced by curcumin.

No MeSH data available.


Related in: MedlinePlus