Memory Disorders https://greenmedinfo.com/category/keywords/Memory%20Disorders en 7 Proven Ways to Keep Your Brain Young https://greenmedinfo.com/blog/7-proven-ways-keep-your-brain-young <div class="copyright">This article is copyrighted by GreenMedInfo LLC, 2024<br/><strong><a href="/greenmedinfocom-re-post-guidelines">Visit our Re-post guidelines</a></strong></div><p class="rtecenter"><img alt="" src="//cdn.greenmedinfo.com/sites/default/files/ckeditor/Sayer Ji/images/chocolate_aging_brain_greenmedinfo.jpg" style="width: 600px; height: 399px;" /></p> <p><em style="font-size: 18px; letter-spacing: 0px;"><strong>Over 5 million Americans have been diagnosed with Alzheimer's. Another 10,000,000 suffer with severe dementia and Parkinson's. Even more struggle with age-related mild cognitive impairment.&nbsp;Here are 7 natural ways to defend your brain.</strong></em></p><p><a href="https://greenmedinfo.com/blog/7-proven-ways-keep-your-brain-young" target="_blank">read more</a></p> https://greenmedinfo.com/blog/7-proven-ways-keep-your-brain-young#comments Aging Aging: Brain Alzheimer's Disease Bacopa Curcumin Dementia Ginkgo biloba Memory Disorders Postmenopausal Disorders: Memory Impairment Turmeric Neuroprotective Agents Aging Alzheimer's disease Bacopa biloba brain CURCUMIN dementia Memory Disorders neuroprotective Neuroprotective Agents prevent brain aging Turmeric Sat, 17 Feb 2024 02:48:05 +0000 GMI reporter 113126 at https://greenmedinfo.com Acute and chronic exercise appears to play a pronounced effect on memory function among young to middle-aged adults. https://greenmedinfo.com/article/acute-and-chronic-exercise-appears-play-pronounced-effect-memory-function-amon n/a PMID:  Am J Health Promot. 2017 Jan 1:890117117737409. Epub 2017 Jan 1. PMID: 29108442 Abstract Title:  The Effects of Exercise on Memory Function Among Young to Middle-Aged Adults: Systematic Review and Recommendations for Future Research. Abstract:  OBJECTIVE: To systematically summarize the experimental effects of exercise on cognitive-related memory function among young to middle-aged adults, which has yet to be done in the literature. DATA SOURCE: PubMed. STUDY INCLUSION AND EXCLUSION CRITERIA: Studies were included if they were published in the English language, indexed in PubMed, employed an experimental study design (eg, traditional parallel group randomized controlled trial: either acute intervention or chronic/training intervention study), and conducted among human adults. Studies were excluded if nonhumans (ie, animal models) were studied, if children/adolescents (&lt;18 years) or older adults (&gt;50 years) were evaluated, and if select chronic diseases (eg, diabetes and dementia) were present. DATA EXTRACTION: A systematic review approach was employed. DATA SYNTHESIS: An extraction table was created synthesizing the key results, and recommendations for future research are emphasized. RESULTS: Among the 17 evaluated studies, 2 were published before the year 2000 (ie, 1998 and 1999), 2 were published in 2007, and the remaining 13 were published in the years 2011 and beyond. This highlights the emergence of this research topic within this age-group (young to middle-aged adults). Among the 17 evaluated studies, 14 were conducted among healthy samples, with 3 conducted among those with a diagnosis of depression. Among the 17 studies, 4 employed a chronic training protocol, with 13 utilizing an acute exercise protocol. Among the 3 experimental studies in the depressed population, all demonstrated a favorable effect of exercise on memory function. Among the 14 trials in the nondepressed population, 10 (71%) demonstrated a favorable effect of exercise on some aspect of memory function. CONCLUSION: Acute and chronic exercise appears to play a pronounced effect on memory function among young to middle-aged adults. Implications and recommendations for future research are outlined in this systematic review. https://greenmedinfo.com/article/acute-and-chronic-exercise-appears-play-pronounced-effect-memory-function-amon#comments Memory Disorders Exercise Neuroprotective Agents exercise Memory Disorders Neuroprotective Agents Review Tue, 09 Jan 2018 16:31:07 +0000 greenmedinfo 158233 at https://greenmedinfo.com Aluminium chloride impairs long-term memory in rats. https://greenmedinfo.com/article/aluminium-chloride-impairs-long-term-memory-rats n/a PMID:  Toxicology. 2014 Sep 2 ;323:95-108. Epub 2014 Jun 25. PMID: 24973631 Abstract Title:  Aluminium chloride impairs long-term memory and downregulates cAMP-PKA-CREB signalling in rats. Abstract:  Epidemiological investigations have indicated that aluminium (Al) is an important environmental neurotoxicant that may be involved in the aetiology of the cognitive dysfunction associated with neurodegenerative diseases. Additionally, exposure to Al is known to cause neurobehavioural abnormalities in animals. Previous studies demonstrated that Al impaired early-phase long-term potentiation (E-LTP) in vivo and in vitro. Our previous research revealed that Al could impair long-term memory via the impairment of late-phase long-term potentiation (L-LTP) in vivo. However, the exact mechanism by which Al impairs long-term memory has been poorly studied thus far. This study was designed not only to observe the effects of subchronic Al treatment on long-term memory and hippocampal ultrastructure but also to explore a possible underlying mechanism (involving the cAMP-PKA-CREB signalling pathway) in the hippocampus of rats.. Pregnant Wistar rats were assigned to four groups. Neonatal rats were exposed to Al by parental lactation for 3 weeks and then fed with distilled water containing 0, 0.2%, 0.4% or 0.6% Al chloride (AlCl3) for 3 postnatal months. The levels of Al in the blood and hippocampus were quantified by atomic absorption spectrophotometry. The shuttle-box test was performed to detect long-term memory. The hippocampus was collected for ultrastructure observation, and the level of cAMP-PKA-CREB signalling was examined. The results showed that the Al concentrations in the blood and hippocampus of Al-treated rats were higher than those of the control rats. Al may impair the long-term memory of rats. Hippocampal cAMP, cPKA, pCREB, BDNF and c-jun expression decreased significantly, and the neuronal and synaptic ultrastructure exhibited pathological changes after Al treatment. These results indicated that Al may induce long-term memory damage in rats by inhibiting cAMP-PKA-CREB signalling and altering the synaptic and neuronal ultrastructure in the hippocampus. https://greenmedinfo.com/article/aluminium-chloride-impairs-long-term-memory-rats#comments Aluminum Toxicity Memory Disorders Aluminum Chloride Aluminum Chloride aluminum toxicity Memory Disorders Animal Study Tue, 23 May 2017 15:07:03 +0000 greenmedinfo 148131 at https://greenmedinfo.com An anthocyanin rich blueberry concentrate improved brain perfusion and activation in brain areas associated with cognitive function. https://greenmedinfo.com/article/anthocyanin-rich-blueberry-concentrate-improved-brain-perfusion-and-activation n/a PMID:  Appl Physiol Nutr Metab. 2017 Mar 1. Epub 2017 Mar 1. PMID: 28249119 Abstract Title:  Enhanced task related brain activation and resting perfusion in healthy older adults after chronic blueberry supplementation. Abstract:  Blueberries are rich in flavonoids, which possess antioxidant and anti-inflammatory properties. High flavonoid intakes attenuate age-related cognitive decline, but data from human intervention studies are sparse. We investigated whether 12 weeks of blueberry concentrate supplementation improved brain perfusion, task-related activation and cognitive function in healthy older adults. Participants were randomised to consume either 30 ml blueberry concentrate providing 387 mg anthocyanidins (5 female, 7 male; age 67.5±3.0 y; BMI, 25.9±3.3 kg.m-2) or isoenergetic placebo (8 female, 6 male; age 69.0 ±3.3 y; BMI, 27.1±.4.0 kg.m-2). Pre- and post-supplementation, participants undertook a battery of cognitive function tests and a numerical Stroop test within a 1.5T MRI scanner while functional magnetic resonanceimages (fMRI) were continuously acquired. Quantitative resting brain perfusion was determined using an arterial spin labelling (ASL) technique, and blood biomarkers of inflammation and oxidative stress were measured. Significant increases in brain activity were observed in response to blueberry supplementation relative to the placebo group within Brodmann areas 4/6/10/21/40/44/45, precuneus, anterior cingulate, and insula/thalamus (p&lt;0.001), as well as significant improvements in grey matter perfusion in the parietal (5.0±1.8 vs -2.9±2.4 %, p=0.013) and occipital (8.0±2.6 vs -0.7±3.2 %, p=0.031) lobes. There was also evidence suggesting improvement in working memory (two back test) after blueberry versus placebo supplementation (p=0.05). Supplementation with an anthocyanin rich blueberry concentrate improved brain perfusion and activation in brain areas associated with cognitive function in healthy older adults. https://greenmedinfo.com/article/anthocyanin-rich-blueberry-concentrate-improved-brain-perfusion-and-activation#comments Blueberry Memory Disorders Anti-Inflammatory Agents Antioxidants Neuroprotective Agents Anti-Inflammatory Agents Antioxidants Blueberry Memory Disorders Neuroprotective Agents Human Study Fri, 03 Mar 2017 23:44:56 +0000 greenmedinfo 144383 at https://greenmedinfo.com Exercise improves recognition memory and synaptic plasticity in the prefrontal cortex for rats modelling vascular dementia. https://greenmedinfo.com/article/exercise-improves-recognition-memory-and-synaptic-plasticity-prefrontal-cortex n/a PMID:  Neurol Res. 2018 Jan ;40(1):68-77. Epub 2017 Nov 10. PMID: 29126372 Abstract Title:  Exercise improves recognition memory and synaptic plasticity in the prefrontal cortex for rats modelling vascular dementia. Abstract:  OBJECTIVES: Functional electrical stimulation (FES) may induce involuntary exercise and make beneficial effects on vascular dementia (VD) by strengthening the BDNF-pCREB-mediated pathway and hippocampal plasticity. Whether FES improves recognition memory and synaptic plasticity in the prefrontal cortex (PFC) was investigated by establishing a VD model. METHODS: The VD rats were administered with two weeks of voluntary exercise, forced exercise, or involuntary exercise induced with FES. Sham-operated and control groups were also included. The behavioral changes were assessed with the novel object recognition test and novel object location test. The expression levels of key proteins related to synaptic plasticity in the PFC were also detected. RESULTS: All types of exercise improved the rats&#039; novel object recognition index, but only voluntary exercise and involuntary exercise induced with FES improved the novel object location index. Any sort of exercise enhanced the expression of key proteins in the PFC. CONCLUSION: Involuntary exercise induced with FES can improve recognition memory in VD better than forced exercise. The mechanism is associated with increased synaptic plasticity in the PFC. FES may be a useful alternative tool for cognitive rehabilitation. https://greenmedinfo.com/article/exercise-improves-recognition-memory-and-synaptic-plasticity-prefrontal-cortex#comments Dementia Memory Disorders Exercise Neuroprotective Agents dementia exercise Memory Disorders Neuroprotective Agents Animal Study Tue, 09 Jan 2018 16:21:42 +0000 greenmedinfo 158230 at https://greenmedinfo.com Naringenin ameliorates learning and memory impairment following systemic lipopolysaccharide challenge. https://greenmedinfo.com/article/naringenin-ameliorates-learning-and-memory-impairment-following-systemic-lipop n/a PMID:  Eur J Pharmacol. 2018 Mar 5. Epub 2018 Mar 5. PMID: 29518393 Abstract Title:  Naringenin ameliorates learning and memory impairment following systemic lipopolysaccharide challenge in the rat. Abstract:  Systemic inflammation following infection is usually associated with long-term complications including cognitive deficit and dementia. Neuroinflammation and cognitive decline are also main hallmarks of several neurological conditions. Naringenin is a citrus flavanone with anti-inflammatory, neuroprotective, and antioxidant potential. In this study, the protective effect of naringenin against lipopolysaccharide (LPS)-induced cognitive decline was evaluated in the rat. LPS was daily injected at a dose of 167μg/kg for 1 week and naringenin was administered p.o. at doses of 25, 50, or 100mg/kg/day. Treatment of LPS-injected rats with naringenin dose-dependently improved spatial recognition memory in Y maze, discrimination ratio in novel object discrimination task, and retention and recall capability inpassive avoidance test. Furthermore, naringenin lowered hippocampal malondialdehyde (MDA) as an index of lipid peroxidation and improved antioxidant defensive system comprising superoxide dismutase (SOD), catalase, and glutathione (GSH) in addition to decreasing acetylcholinesterase (AChE) activity.Additionally, naringenin was able to lower hippocampal nuclear factor-kappaB (NF-κB), toll-like receptor 4 (TLR4), tumor necrosis factor α (TNFα), cyclooxygenase-2 (COX2), inducible nitric oxide synthase (iNOS), glial fibrillary acidic protein (GFAP) level and its immunoreactivity, and to elevate nuclear factor (erythroid-derived 2)-like 2 (Nrf2). Taken together, naringenin could alleviate LPS-induced cognitive deficits and neuroinflammation, as was evident from attenuation of oxidative stress and AChE and modulation of Nrf2/NF-κB/TNFα/COX2/iNOS/TLR4/GFAP. https://greenmedinfo.com/article/naringenin-ameliorates-learning-and-memory-impairment-following-systemic-lipop#comments Lipopolysaccharide-Induced Toxicity Memory Disorders Naringenin Anti-Inflammatory Agents Cyclooxygenase 2 Inhibitors Neuroprotective Agents NF-kappaB Inhibitor Nrf2 activation Tumor Necrosis Factor (TNF) Alpha Inhibitor Anti-Inflammatory Agents Lipopolysaccharide-Induced Toxicity Memory Disorders Naringenin Animal Study Sat, 10 Mar 2018 03:05:12 +0000 greenmedinfo 161004 at https://greenmedinfo.com Oligonol improves Aβ(25-35)-induced memory deficit and cognition impairment. https://greenmedinfo.com/article/oligonol-improves-25-35-induced-memory-deficit-and-cognition-impairment n/a PMID:  Nutr Res. 2014 Jul ;34(7):595-603. Epub 2014 Jun 14. PMID: 25150118 Abstract Title:  Oligonol improves memory and cognition under an amyloidβ(25-35)-induced Alzheimer&#039;s mouse model. Abstract:  Alzheimer&#039;s disease is an age-dependent progressive neurodegenerative disorder that results in impairments of memory and cognitive function. It is hypothesized that oligonol has ameliorative effects on memory impairment and reduced cognitive functions in mice with Alzheimer&#039;s disease induced by amyloidβ(25-35) (Aβ(25-35)) injection. The protective effect of an oligonol against Aβ(25-35)-induced memory impairment was investigated in an in vivo Alzheimer&#039;s mouse model. The aggregation of Aβ25-35 was induced by incubation at 37°C for 3 days before injection into mice brains (5 nmol/mouse), andthen oligonol was orally administered at 100 and 200 mg/kg of body weight for 2 weeks. Memory and cognition were observed in T-maze, object recognition, and Morris water maze tests. The group injected with Aβ(25-35) showed impairments in both recognition and memory. However, novel object recognition and new route awareness abilities were dose dependently improved by the oral administration of oligonol. In addition, the results of the Morris water maze test indicated that oligonol exerted protective activity against cognitive impairment induced by Aβ(25-35). Furthermore, nitric oxide formation and lipid peroxidation were significantly elevated by Aβ(25-35), whereas oligonol treatment significantly decreased nitric oxide formation and lipid peroxidation in the brain, liver, and kidneys. The present results suggest that oligonol improves Aβ(25-35)-induced memory deficit and cognition impairment. https://greenmedinfo.com/article/oligonol-improves-25-35-induced-memory-deficit-and-cognition-impairment#comments Lipid Peroxidation Lychee Memory Disorders Antioxidants Neuroprotective Agents Nitric Oxide Inhibitor Antioxidants Lipid Peroxidation Lychee Memory Disorders Phytotherapy Plant Extracts Animal Study Tue, 04 Apr 2017 19:18:52 +0000 greenmedinfo 145893 at https://greenmedinfo.com Pine needle extract prevents hippocampal memory impairment in acute restraint stress mouse model. https://greenmedinfo.com/article/pine-needle-extract-prevents-hippocampal-memory-impairment-acute-restraint-str n/a PMID:  J Ethnopharmacol. 2017 Jun 19 ;207:226-236. Epub 2017 Jun 19. PMID: 28642096 Abstract Title:  Pine needle extract prevents hippocampal memory impairment in acute restraint stress mouse model. Abstract:  ETHNOPHARMACOLOGICAL RELEVANCE: The Pinus densiflora leaf has been traditionally used to treat mental health disorders as a traditional Chinese medicine. Here we examined the ethnopharmacological relevance of pine needle on memory impairment caused by stress. AIM OF THE STUDY: To elucidate the possible modulatory actions of 30% ethanolic pine needle extract (PNE) on stress-induced hippocampal excitotoxicity, we adopted an acute restraint stress mouse model. MATERIALS AND METHODS: Mice were orally administered with PNE (25, 50, or 100mg/kg) or ascorbic acid (100mg/kg) for 9 days, and were then subjected to restraint stress (6h/day) for 3 days (from experimental day 7-9). To evaluate spatial cognitive and memory function, the Morris water maze was performed during experimental days 5-9. RESULTS: Restraint stress induced the memory impairment (the prolonged escape latency and cumulative path-length, and reduced time spent in the target quadrant), and these effects were significantly prevented by PNE treatment. The levels of corticosterone and its receptor in the sera/hippocampus were increased by restraint stress, which was normalized by PNE treatment. Restraint stress elicited the hippocampal excitotoxicity, the inflammatory response and oxidative injury as demonstrated by the increased glutamate levels, altered levels of tumor necrosis factor (TNF)-α and imbalanced oxidant-antioxidant balance biomarkers. Two immunohistochemistry activities against glial fibrillary acidic protein (GFAP)-positive astrocytes and neuronal nuclei (NeuN)-positive neurons supported the finding of excitotoxicity especially in the cornu ammonis (CA)3 region of the hippocampus. Those alterations were notably attenuated by administration of PNE. CONCLUSIONS: The above findings showed that PNE has pharmacological properties that modulate the hippocampal excitotoxicity-derived memory impairment under severe stress conditions. https://greenmedinfo.com/article/pine-needle-extract-prevents-hippocampal-memory-impairment-acute-restraint-str#comments Memory Disorders Pine Needle Neuroprotective Agents Memory Disorders Neuroprotective Agents Pine Needle Plant Extracts Animal Study Tue, 11 Jul 2017 17:57:40 +0000 greenmedinfo 150283 at https://greenmedinfo.com Spirulina maxima administered together with other therapeutics may induce synergistic effects to ameliorate cognitive dysfunction. https://greenmedinfo.com/article/spirulina-maxima-administered-together-other-therapeutics-may-induce-synergist n/a PMID:  Int J Mol Sci. 2017 Nov 13 ;18(11). Epub 2017 Nov 13. PMID: 29137190 Abstract Title:  Spirulina maxima Extract Ameliorates Learning and Memory Impairments via Inhibiting GSK-3β Phosphorylation Induced by Intracerebroventricular Injection of Amyloid-β 1-42 in Mice. Abstract:  Spirulina maxima, a microalga containing high levels of protein and many polyphenols, including chlorophyll a and C-phycocyanin, has antioxidant and anti-inflammatory therapeutic effects. However, the mechanisms where by Spirulina maxima ameliorates cognitive disorders induced by amyloid-β 1-42 (Aβ1-42) are not fully understood. In this study, we investigated whether a 70% ethanol extract of Spirulina maxima (SM70EE) ameliorated cognitive impairments induced by an intracerebroventricular injection of Aβ1-42 in mice. SM70EE increased the step-through latency time in the passive avoidance test and decreased the escape latency time in the Morris water maze test in Aβ1-42-injected mice. SM70EE reduced hippocampal Aβ1-42 levels and inhibited amyloid precursor protein processing-associated factors in Aβ1-42-injected mice. Additionally, acetylcholinesterase activity was suppressed by SM70EE in Aβ1-42-injected mice. Hippocampal glutathione levels were examined to determine the effects of SM70EE on oxidative stress in Aβ1-42-injected mice. SM70EE increased the levels of glutathione and its associated factors that were reduced in Aβ1-42-injected mice. SM70EE also promotedactivation of the brain-derived neurotrophic factor/phosphatidylinositol-3 kinase/serine/threonine protein kinase signaling pathway and inhibited glycogen synthase kinase-3β phosphorylation. These findings suggested that SM70EE ameliorated Aβ1-42-induced cognitive impairments by inhibiting the increased phosphorylation of glycogen synthase kinase-3β caused by intracerebroventricular injection of Aβ1-42 in mice. https://greenmedinfo.com/article/spirulina-maxima-administered-together-other-therapeutics-may-induce-synergist#comments Alzheimer's Disease Memory Disorders Spirulina Brain-derived neurotrophic factor modulator Neuroprotective Agents Alzheimer's disease Brain-derived neurotrophic factor modulator Memory Disorders Neuroprotective Agents Spirulina Animal Study Thu, 07 Dec 2017 08:55:22 +0000 greenmedinfo 157098 at https://greenmedinfo.com These findings showed that aluminum exposure caused spatial memory damage. https://greenmedinfo.com/article/these-findings-showed-aluminum-exposure-caused-spatial-memory-damage n/a PMID:  J Toxicol Sci. 2013 ;38(2):255-68. PMID: 23535404 Abstract Title:  Effects of subchronic aluminum exposure on spatial memory, ultrastructure and L-LTP of hippocampus in rats. Abstract:  Epidemiological investigations have indicated that aluminum (Al), as an important environmental neurotoxicant, could cause damage to the cognitive function which was closely related with neurodegenerative diseases. Long-term potentiation (LTP) is one form of synaptic plasticity in association with cognitive function. Previous studies have demonstrated that Al impaired early phase long-term potentiation (E-LTP) in vivo and in vitro. However, Al-induced damage to late phase long-term potentiation (L-LTP) has poorly been studied. The present study was designed to observe the effects of subchronic Al exposure on the spatial memory, hippocampus ultrastructure and L-LTP in rats. Pregnant Wistar rats were assigned to four groups. Neonatal rats were exposed to Al by parental lactation from parturition to weaning for 3 weeks and then fed with the distilled water containing 0, 0.2%, 0.4% and 0.6% aluminum chloride (AlCl3) respectively from weaning to postnatal 3 months. The levels of Al in blood and hippocampus were quantitated by atomic absorption spectrophotometer. Morris water maze test was performed to study spatial memory. The induction and maintenance of L-LTP in area of Schaffer collateral- CA1 synapse was recorded by extracellular microelectrode recording technology in hippocampus of experimental rats. Hippocampus was collected for transmission electron microscopy observation. The results showed that the Al concentrations in blood and hippocampus of Al-exposed rats were higher than those of the control rats. Al could impair spatial memory ability of rats. Neuronal and synaptic ultrastructure from Al-exposed rats presented pathological changes; the incidence of L-LTP has a decrease trend while population spike (PS) amplitude was much smaller significantly stimulated by high-frequency stimulation (HFS) in Al-exposed rats. Our findings showed that Al exposure caused spatial memory damage, under which the neuronal and synaptic ultrastructure changes maybe were their morphological basis and the impaired L-LTP of hippocampus could be their electrophysiological basis. https://greenmedinfo.com/article/these-findings-showed-aluminum-exposure-caused-spatial-memory-damage#comments Aluminum Toxicity Memory Disorders Aluminum aluminum aluminum toxicity Memory Disorders Animal Study In Vitro Study Tue, 23 May 2017 14:16:06 +0000 greenmedinfo 148126 at https://greenmedinfo.com These results indicate that SIRT1 and TORC1 might play an important mediating role in aluminium -induced long-term memory impairment. https://greenmedinfo.com/article/these-results-indicate-sirt1-and-torc1-might-play-important-mediating-role-alu n/a PMID:  Basic Clin Pharmacol Toxicol. 2017 Oct ;121(4):342-352. Epub 2017 Jun 19. PMID: 28429887 Abstract Title:  Effects of Aluminium on Long-Term Memory in Rats and on SIRT1 Mediating the Transcription of CREB-Dependent Gene in Hippocampus. Abstract:  Epidemiological investigations have shown that aluminium (Al) is an important neurotoxicant which can be absorbed by organisms via various routes. Previous studies have confirmed that exposure to Al could cause neurodegenerative diseases, decline CREB phosphorylation and then down-regulate the transcription and protein expression of its target genes including BDNF. However, recent studies revealed that CREB activation alone was far from enough to activate the expression of long-term memory (LTM)-related genes; there might be other regulatory factors involved in this process. Several studies showed that TORC1 might be involved in regulating the transcription of downstream target genes as well. Also, TORC1 could be mediated by SIRT1 during the formation of LTM. However, the role of CREB regulating system in Al-induced LTM impairment was still not utterly elucidated till now. This study was designed to establish the rat model of subchronic Al exposure to observe the neuroethology, regulatory factor levels and molecular biological alterations in hippocampal cells. The results showed that, with the increasing AlCl3 dose, blood Al content increased gradually; morphology of the hippocampus and neuronal ultrastructure were aberrant; in the Morris water maze test, the escape latency and distance travelled became longer, swimming traces turned more complicated in the place navigation test; intracellular Ca2+ , cAMP levels declined significantly in AlCl3 -treated rats, followed by abated nuclear translocation of TORC1 and decreased SIRT1, TORC1 and pCREB levels. These results indicate that SIRT1 and TORC1 might play an important mediating role in Al-induced LTM impairment. https://greenmedinfo.com/article/these-results-indicate-sirt1-and-torc1-might-play-important-mediating-role-alu#comments Aluminum Toxicity Memory Disorders Neurodegenerative Diseases Aluminum aluminum aluminum toxicity Memory Disorders Neurodegenerative diseases Animal Study Thu, 08 Feb 2018 01:23:31 +0000 greenmedinfo 159467 at https://greenmedinfo.com