Molecular Chaperone Dysfunction in Neurodegenerative Diseases and Effects of Curcumin

Figure 1

Protein misfolding and aggregation in different neurodegenerative diseases. (a) Schematic diagram showing steps of formation of different abnormal protein species after the cellular stress response; (b) schematic diagram of sequential formation of different amyloid species; (c) electron micrographs of different species of amyloid beta protein; (d) amyloid beta plaques (upper) stained with 4G8 antibody from brain tissue of AD mouse model, neurofibrillary tangle (middle), and synaptic (dendritic spine, Golgi-Cox stain) loss in mouse model of Alzheimer’s disease (lower); (e) tyrosine hydroxylase (the indicator of dopaminergic neuron) positive (small arrow) neuronal loss in the substantia nigra pars compacta and tyrosine hydroxylase positive fibre loss in the striatum of MPTP-model of Parkinson’s disease.

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