Neuroprotective potential of Aqueous Cinnamon Extract on cerebellar Amyloid-β plaques in Alzheimer's Disease [P2-E/4] (original) (raw)
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Neuro-amelioration of cinnamaldehyde in aluminum-induced Alzheimer's disease rat model
Journal of Histotechnology, 2019
Aluminum (Al) is a neurotoxic substance which has played an important role in the etiology, pathogenesis, and development of amyloid-β (Aβ) plaques. This study was carried out to evaluate the neuroprotective effect of aqueous cinnamon extract against aluminum chloride (AlCl3)-induced Alzheimer’s disease. Forty adult male albino rats, randomly divided into four equal groups. Control group; ACE200 group administered aqueous cinnamon extract (ACE) orally; AlCl3 group received daily intraperitoneal (i.p.) injection of AlCl3 for 60 days to induce neurotoxicity and AlCl3 + ACE200 group received a combination of AlCl3 and ACE in the same dose and route as previous groups. Aluminum administration significantly enhanced the memory impairment and the Aβ formation in the rat model. The cerebellum exhibited a significant reduced number of Purkinje cells, marked decrease in the density of dendritic arborization and prominent perineuronal spaces in the molecular layer. There was loss of dendritic spines, neurofibrillary degeneration, and appearance of neuritic plaques. Concomitant administration of AlCl3 and ACE displayed an observable protection against these changes with progressive improvement in memory and intellectual performance. In conclusion, ACE may play a protective role against formation of amyloid-β plaques in cerebellum. KEYWORDS: Alzheimer, aluminum chloride, cinnamon, memory, amyloid beta, apoptosis
Journal of Alzheimer's disease : JAD, 2003
The effect of chronic aluminum intake has been investigated in the brain of aged male Wistar rats to assess the potential role of the accumulation of this metal ion on the development of neurodegenerative features observed in Alzheimer's disease. AlCl3 x 6 H2O (2g/L) was administered to experimental animals for 6 months in the drinking water. The total content of Al (microg/g fresh tissue) was measured by inductively coupled plasma atomic emission spectrometry (ICP-AES), while the content of Cu, Zn and Mn was determined by flame AAS in the prosencephalon + mesencephalon, pons-medulla and cerebellum of control and Al(III)-treated animals. The area occupied by mossy fibres in the CA3 field of the hippocampus was estimated by a computer-assisted morphometric method following Timm's preferential staining. In Al(III)-treated rats the concentration of Cu, Zn and Mn did not increase significantly (p < 0.5) in prosencephalon + mesencephalon, nor in pons-medulla (p < 0.5) excep...
Aluminium and Neuro-degeneration: Mechanism of Pathogenesis and Possible Strategies for Mitigation
One of the most abundant metal in our environment is aluminium (Al). Occupational exposure of humans to Al takes place during its extractions, processing and fabrications of articles of daily use. Al in drinking water and as well as its use in packaging & storage of food is also a potential source of exposure. Acute exposure of higher concentration or chronic exposure of low concentration of Al leads to its aggregation in various parts of the body, resulting in system toxicity. Brain is highly susceptible to Al accumulation toxicity. In humans, exposure of Al is a risk factor for the starting of Alzheimer Disease. The adverse effect of Al exposure on nervous system results in memory loss, balance problems and impairment of coordination. High level of Al in brain increases lipid peroxidation and oxidative stress and reduces antioxidant enzymes level. It also causes aggregation of amyloid beta proteins and formation of Neurofibrillary Tangles (NFTs) of tau proteins which finally leads to death of neuronal cell and neurotoxicity. Metabolism and excretion of heavy metals including Al is very difficult and its leads to accumulation. The chelation therapy has been proposed where the organic molecules like EDTA, Chlorogenic acid and GSH binds with the heavy metals and facilitates for their excretion from body. However, non-specific binding of these chelators is another major safety concern. Medicinal plants and their phytochemicals with multiple mechanism of action have been proposed as a very good alternative for ameliorating heavy metal induced toxicity. In addition to mild chelating activities, the phytochemicals have antioxidant, anti-inflammatory, cytokine modulatory and other specific actions for proving holistic neuro-protection on heavy metal exposure.
Aluminum and Alzheimer's disease: a new look
Journal of Alzheimer's disease : JAD, 2006
Despite the circumstantial and sometimes equivocal support, the hypothetic involvement of aluminum (Al) in the etiology and pathogenesis of Alzheimer's disease (AD) has subsisted in neuroscience. There are very few other examples of scientific hypotheses on the pathogenesis of a disease that have been revisited so many times, once a new method that would allow a test of Al's accumulations in the brain of AD patients or a comparison between Al-induced and AD neuropathological signs has become available. Although objects of methodological controversies for scientists and oversimplification for lay spectators, several lines of evidence have strongly supported the involvement of Al as a secondary aggravating factor or risk factor in the pathogenesis of AD. We review evidence on the similarities and dissimilarities between Al-induced neurofibrillary degeneration and paired helical filaments from AD, the accumulation of Al in neurofibrillary tangles and senile plaques from AD, the...
Journal of Alzheimer's disease : JAD, 2010
In recent years, interest in the potential role of metals in the pathogenesis of Alzheimer's disease (AD) has grown considerably. In particular, aluminum (Al) neurotoxicity was suggested after its discovery in the senile plaques and neurofibrillary tangles that represent the principal neuropathological hallmarks of AD. Al is omnipresent in everyday life and can enter the human body from several sources, most notably from drinking water and food consumption. The evidence supporting association from ingestion of Al from drinking water is somewhat stronger than for its ingestion from food. However, other elements present in drinking water, such as fluoride, copper, zinc, or iron could also have an effect on cognitive impairment or modify any Al neurotoxicity. Some epidemiological studies, but not all, suggested that silica could be protective against Al damage, because it reduces oral absorption of Al and/or enhances Al excretion. Some epidemiological investigations suggested an as...
Aluminium in Alzheimer’s disease: are we still at a crossroad
Experientia, 2005
Aluminium, an environmentally abundant non-redox trivalent cation has long been implicated in the pathogenesis of Alzheimer’s disease (AD). However, the definite mechanism of aluminium toxicity in AD is not known. Evidence suggests that trace metal homeostasis plays a crucial role in the normal functioning of the brain, and any disturbance in it can exacerbate events associated with AD. The present paper reviews the scientific literature linking aluminium with AD. The focus is on aluminium levels in brain, region-specific and subcellular distribution, its relation to neurofibrillary tangles, amyloid beta, and other metals. A detailed mechanism of the role of aluminium in oxidative stress and cell death is highlighted. The importance of complex speciation chemistry of aluminium in relation to biology has been emphasized. The debatable role of aluminium in AD and the cross-talk between aluminium and genetic susceptibility are also discussed. Finally, it is concluded based on extensive literature that the neurotoxic effects of aluminium are beyond any doubt, and aluminium as a factor in AD cannot be discarded. However, whether aluminium is a sole factor in AD and whether it is a factor in all AD cases still needs to be understood.