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Authors: Huang, Han-Chang | Jiang, Zhao-Feng

Article Type: Review Article

Abstract: The neuropathology associated with Alzheimer's disease (AD) is characterized by the presence of extracellularly neuritic plaques, intracellularly neurofibrillary tangles and the loss of basal forebrain cholinergic neurons. The neuritic plaque is composed of a core of amyloid-β peptide (Aβ) while the neurofibrillary tangles contain phosphorylated tau protein, and, as such, both Aβ and tau are important molecules associated with AD. In healthy human bodies, clearance mechanisms for Aβ are available; yet if clearance fails, Aβ accumulates, increasing the risk of neurotoxicity in the brain. Tau, one of the main microtubule-associated proteins, will be hyperphosphorylated and lose the ability to bind …microtubules when the homeostasis of phosphorylation and dephosphorylation is disturbed in neurons. Accumulated Aβ and hyperphosphorylated tau are thought to be coexistent. Research on the pathological changes in AD indicates that accumulated Aβ in vivo may initiate the hyperphosphorylation of tau. Also, the signal transduction pathways of tau hyperphosphorylation may be related to accumulated Aβ. In this review, we will discuss how Aβ accumulates, how tau protein is hyperphosphorylated, and how accumulated Aβ initiates hyperphosphorylation of tau protein in AD. Show more

Keywords: α7nAChR, amyloid-β peptide (Aβ), oxidative stress, PI3K/Akt, tau protein

DOI: 10.3233/JAD-2009-0960

Citation: Journal of Alzheimer's Disease, vol. 16, no. 1, pp. 15-27, 2009

Authors: Huang, Han-Chang | Jiang, Zhao-Feng

Article Type: Review Article

Abstract: Alzheimer's disease (AD) is one of the most common forms of neurodegenerative disease. Amyloid-β peptide (Aβ) is the most crucial molecule related to the pathological development of AD. Amyloid-β protein precursor (AβPP) is one of AβPP family members with conserved type I transmembrane. The genetic mutations of AβPP and the abnormity of its post-transcription and proteolytic processing contribute to the elevation of Aβ. The accumulation of Aβ in senile plaques is believed to be the most important event in AD pathology. Therefore, as a key upstream molecule of Aβ, AβPP is related to the AD pathology, but the biological function …of AβPP is still not fully clear. AβPP-like proteins are widely expressed in multicellular eukaryotes. AβPP-like homologous genes and proteins are highly conserved in various organisms from invertebrates to mammals. AβPP-like genes undergo similarly pathways of transcription and post-transcription processing, and AβPP-like proteins is proteolyzed by the similar α-cleavage and the β-cleavage pathways. Based on the homology and the resemble domains, AβPP may play similar roles in organisms. In this article, we reviewed homology and structures of AβPP family members in organisms and further discussed potential biological function in normal and AD brains. Show more

Keywords: Alzheimer's disease, amyloid-β protein precursor, biological function, homology, structure

DOI: 10.3233/JAD-2011-110335

Citation: Journal of Alzheimer's Disease, vol. 26, no. 4, pp. 607-626, 2011

Authors: Huang, Han-Chang | Xu, Ke | Jiang, Zhao-Feng

Article Type: Research Article

Abstract: The deposition of amyloid-β (Aβ) peptides in senile plaques is one of pathological hallmarks of Alzheimer's disease (AD). Mitochondrial dysfunction is an early event of cell apoptosis. Increasing evidence indicates that Aβ induces neuronal apoptosis through mitochondrial dysfunction. Curcumin, an anti-oxidative component of turmeric (Curcuma longa), has shown anti-tumor, anti-inflammatory, and anti-oxidative properties. In this study, we investigated the protective effects of curcumin against mitochondrial dysfunction induced by Aβ. Based on the assay results of mitochondrial metabolic markers, we found that curcumin protects human neuroblastoma SH-SY5Y cells against the Aβ-induced damage of mitochondrial energy metabolism. Curcumin inhibits Aβ-induced mitochondrial depolarization …of membrane potential (Δψm ) and suppresses mitochondrial apoptosis-related proteins including cytochrome c, caspase-3, and Bax, which are activated by Aβ. Aβ-induced disturbances of redox state are linked to mitochondrial dysfunction. Curcumin normalizes cellular antioxidant enzymes (including SOD and catalase) in both protein expression and activity and decreases oxidative stress level in Aβ-treated cells. Both total GSK-3β expression and phospho-Ser9 GSK-3β (pSer9-GSK-3β) are down-regulated in the cells pre-treated with curcumin. This study demonstrates curcumin-mediated neuroprotection against Aβ-induced mitochondrial metabolic deficiency and abnormal alteration of oxidative stress. Inhibition of GSK-3β is involved in the protection of curcumin against Aβ-induced mitochondrial dysfunction. Show more

Keywords: Alzheimer's disease, amyloid-β, curcumin, glycogen synthase kinase-3β, mitochondrial dysfunction, reactive oxygen species

DOI: 10.3233/JAD-2012-120688

Citation: Journal of Alzheimer's Disease, vol. 32, no. 4, pp. 981-996, 2012

Authors: Yang, Xiao-Hui | Huang, Han-Chang | Chen, Lin | Xu, Wei | Jiang, Zhao-Feng

Article Type: Research Article

Abstract: Cu(II) has been shown in vitro to profoundly promote the aggregation of amyloid-β peptide (Aβ, a key pathological event in Alzheimer's disease. We investigated both the effect of Cu(II) on the secondary structure transformation of Aβ and the probable residues involved in the chelation to Cu(II). The effects of Cu(II) on Aβ was analyzed by the circular dichroism spectra, Th-T fluorescence and sedimentation assay, and the results indicated that Cu(II) could disrupt the already formed β-sheet structure, convert β-sheeted aggregates into non-β-sheeted aggregates and promote oligomeric Aβ to precipitate in a non-β-sheeted aggregation way. Additionally, we confirmed that the function …of Cu(II) discussed above was achieved through its interaction with His6, His13, and His14 by investigating an Aβ mutant, 23,6,13,14 Aβ1-40 . Show more

Keywords: Alzheimer's disease, amyloid-β peptide, β-sheet structure, copper

DOI: 10.3233/JAD-2009-1186

Citation: Journal of Alzheimer's Disease, vol. 18, no. 4, pp. 799-810, 2009

Authors: Huang, Han-Chang | Zheng, Bo-Wen | Guo, Yu | Zhao, Jian | Zhao, Jiang-Yan | Ma, Xiao-Wei | Jiang, Zhao-Feng

Article Type: Research Article

Abstract: Epidemiological data imply links between the increasing incidences of Alzheimer’s disease (AD) and type 2 diabetes mellitus. In this study, an AD rat model was established by combining treatments with intracerebroventricular streptozotocin (icv-STZ) and subcutaneous D-galactose, and the effects of curcumin on depressing AD-like symptoms were investigated. In the AD model group, rats were treated with icv-STZ in each hippocampus with 3.0 mg/kg of bodyweight once and then were subcutaneously injected with D-galactose daily (125 mg/kg of bodyweight) for 7 weeks. In the curcumin-protective group, after icv-STZ treatment, rats were treated with D-galactose (the same as in the AD model group) and …intraperitoneally injected with curcumin daily (10 mg/kg of bodyweight) for 7 weeks. Vehicle-treated rats were treated as control. Compared with the vehicle control, the amount of protein carbonylation and glutathione in liver, as well as malondialdehyde in serum, were upregulated but glutathione peroxidase activity in blood was downregulated in the AD model group. The shuttle index and locomotor activity of rats in the AD model group were decreased compared with the vehicle control group. Furthermore, AD model rats showed neuronal damage and neuron loss with formation of amyloid-like substances and neurofibrillary tangles, and the levels of both β-cleavage of AβPP and phosphorylation of tau (Ser396) were significantly increased compared with the vehicle control group. Notably, compared with the AD model group, oxidative stress was decreased and the abilities of active avoidance and locomotor activity were improved, as well as attenuated neurodegeneration, in the curcumin-protective group. These results imply the applications of this animal model for AD research and of curcumin in the treatment of AD. Show more

Keywords: Alzheimer’s disease, animal model, curcumin, D-galactose, neurodegeneration, streptozotocin

DOI: 10.3233/JAD-150872

Citation: Journal of Alzheimer's Disease, vol. 52, no. 3, pp. 899-911, 2016