Potential-treatment-of-Alzheimer’s-disease-using-curcumin

7/28/2019 Potential-treatment-of-Alzheimers-disease-using-curcumin

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Potential treatment of Alzheimers disease

using curcumin

What is Alzheimers?

Alzheimers disease (AD) is a progressive neurodegenerative disease. It is characterized by

progressive cognitive degeneration together with declining activities of daily living and

behavioral changes. It is common type of pre-senile and senile dementia. According to world

health organization (WHO).5% of men and women of above 60 years are affected with

Alzheimers type dementia worldwide. Alzheimers disease was discovered in 1907 by Dr.Alois

Alzheimer, a German medical researcher who described a unique and destructive pathology in

his patients brains.AD primarily involves the parts of brain that control thought, memory, and

language.ad evolves slowly. At first its only symptom may be mild forgetfulness. As the disease

progress more serious symptoms arise


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NEUROPATHOLOGY:

1. The pathology of brain exhibiting the disease shows two distinct characteristics that result in

major neuronal loss.

2. These include extra cellular plaques and intracellular tangles found in the hippocampus,cerebral cortex, and other areas that are crucial for cognitive functioning.

3. Plaques are formed mostly from the deposition of beta amyloid. a beta is formed after

sequential deavage of the amyloidal precursor protein(app), a transmembrane glycoprotein that

penetrates through the neuronal membrane. App is critical to neuron growth, survival and post-

inquiry repair.

4. In AD an unknown process causes APP to be divided into smaller fragments by enzymes

through proteolysis.

5. Tangles are formed from paired helical filaments composed of neuro filament andhyperphosphorelated tau protein.

6. There is an increased presence of monocytes/macrophages in the cerebral vessel wall and

reactive or activated microglia cells in the adjacent parenchyma

7. Amyloid plaques are known to cause oxidative damage in the brains of Alzheimers sufferers.

8. Free radicals generated by beta amyloid and other factors and other factors, such as

mitochondrial abnormalities in cells, inadequate energy supply, inflammation, or abnormal

changes in natural antioxidant defenses, may play a role in the pathophysiology of AD.


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Studies on CURCUMIN:

1. Effects of curcumin were observed in an animal model of AD in which human A140 and

A142 were infused with a lipoprotein chaperone into the cerebral ventricles of aged

female rats.2. Such rats develop A deposits, neurodegeneration, and memory impairment. Reduced

levels of 8-EPI-F2 isoprostanes, an oxidative produce of arachidonic acid, and normal

levels of synaptophysin, a marker of synaptic integrity were seen in curcumin (2000ppm), but not ibuprofen-fed rats. Both curcumin and ibuprofen-fed rats had decreased

microglial activity. Increased microglial staining was seen in areas surrounding amyloid

plaques.3. Measurement of the spatial memory and post-synaptic density 95 (PSD-95) levels, a

synaptic protein that anchors N-methyl-D-aspartate (NMDA) receptors, in the brains of

younger rats infused with a higher dose of A140 and A142 was done, Rats fed withcurcumin (500 ppm) showed reduced path length and latency in finding the hidden

platform in the Morris water maze test, demonstrating superior memory functioncompared to control-fed rats

4. Increased PSD-95 and decreased A-stained area also were seen in curcumin-fed rats.These studies suggest that curcumin ameliorates both the pathology and cognitive deficits

induced by A infusion in rats.

These findings provide evidence that curcumin can ameliorate the pathology and cognitive

deficits in animal models of AD.


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2. Subsequently performed fluorescence studies demonstrate that curcumin binds to

amyloid plaques in human AD and Tg2576 transgenic mouse brain tissue in-vitro.3. Furthermore, curcumin was found to bind to amyloid plaques when such mice were either

fed curcumin or curcumin injected in the carotid artery.

4. Curcumin was a better A-beta 40 aggregation inhibitor and it destabilizes the A-beta

polymer. Inin vitro

studies, curcumin inhibits aggregation as well as disaggregates toform fibrillar A-beta 40.

5. studies showed that using fluorescence spectroscopic analysis with thioflavin T and

electron microscopic studies, curcumin destabilizes the fA-beta(1-40) and fA-beta(1-42)as well as their extension. .Curcumin-derived isoxazoles and pyrazoles bind to the

amyloid beta peptide (Abeta) and inhibit amyloid precursor protein (APP) metabolism.

6. Curcumin given to APPswe/PS1dE9 mice for 7 days crosses the blood-brain barrier as

demonstrated by multi-photon microscopy and reduces the existing senile plaques.

ADVANTAGES:

1. Curcumin scores over NSAIDS due to its multipronged action.

2. Long-term use of NSAIDS leads to complications like hepatotoxicity which is not seen in

curcumin.


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3. Even if used for long periods it doesnt it doesnt produce side effects.

4. USFDA has classified curcumin as GRAS- generally recognized as safe.

CONCLUSION:

Based on the main findings detailed above, curcumin will lead to a promising treatment

for AD & a particularly promising natural agent in fighting the ravages of aging and

degenerative diseases.

The clinically studied chemical properties of curcumin and its various effects an AD shows the

possibility to do further research and develop better drugs based on curcumin for treating AD.

References:

1. Harrington Charles, Rickard Janet E, Horsley David, et al (July 2008). "Methylthioniniumchloride (MTC) acts as a Tau aggregation inhibitor (TAI) in a cellular model and reverses Tau

pathology in transgenic mouse models of Alzheimer's disease". Alzheimer's & Dementia

(Alzheimers Association)

2. Hawkes CA, McLaurin J (November 2007). "Curcumin for Alzheimer's disease". Expert RevNeurother.

Document BySANTOSH BHARADWAJ REDDYEmail: [email protected]

Engineeringpapers.blogspot.com
mailto:[email protected]:[email protected]


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