Article
Plant Sciences
Caixia Zang, Hui Liu, Junmei Shang, Hanyu Yang, Lu Wang, Chanjuan Sheng, Zihong Zhang, Xiuqi Bao, Yang Yu, Xinsheng Yao, Dan Zhang
Summary: The study demonstrates that GJ-4 improves cognitive deficits in APP/PS1 transgenic mice by reducing A beta levels, inhibiting tau protein phosphorylation, and suppressing neuroinflammatory responses. These findings provide a basis for further development of GJ-4 as a potential treatment for AD.
Article
Biochemistry & Molecular Biology
Seda Onder, Kevser Biberoglu, Melike Yuksel, Ozden Tacal
Summary: Alzheimer's disease is characterized by amyloid plaques, neurofibrillary tangles, and neuronal loss. Recent studies focus on multi-targeted drug strategies. TBO, a potential candidate, shows promising effects on reducing amyloid levels and decreasing phosphorylated tau.
CHEMICO-BIOLOGICAL INTERACTIONS
(2022)
Article
Biochemistry & Molecular Biology
Jiang Chen, Anran Fan, Song Li, Yan Xiao, Yanlin Fu, Jun-Sheng Chen, Dan Zi, Ling-Hui Zeng, Jun Tan
Summary: Alzheimer's disease (AD), the most common type of dementia, is characterized by the presence of extracellular senile plaques composed of beta-amyloid peptides and intracellular neurofibrillary tangles containing phosphorylated-tau protein. This study has demonstrated the interaction between soluble tau and the N-terminal of amyloid precursor protein (APP) in vitro and in vivo, as well as the involvement of APP in the cellular uptake of tau through endocytosis. Targeting the pathological interaction between N-terminal APP and tau could be a promising therapeutic strategy for AD.
CELLULAR AND MOLECULAR LIFE SCIENCES
(2023)
Review
Biochemistry & Molecular Biology
Huiqin Zhang, Wei Wei, Ming Zhao, Lina Ma, Xuefan Jiang, Hui Pei, Yu Cao, Hao Li
Summary: Extracellular neuritic plaques and intracellular neurofibrillary tangles, composed of amyloid-beta and phosphorylated tau protein respectively, are hallmark proteins of Alzheimer's disease. The interactions between these proteins have been extensively studied, with A beta accelerating tau phosphorylation, tau mediating A beta toxicity, and potential synergistic effects on microglial cells and astrocytes. Understanding these interactions may lead to new interventions against Alzheimer's disease.
INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
(2021)
Review
Pharmacology & Pharmacy
Mohammad Rafi Khezri, Keyvan Yousefi, Negin Mahboubi, Darya Hodaei, Morteza Ghasemnejad-Berenji
Summary: Alzheimer's disease (AD) is a common neurodegenerative disorder worldwide, and its association with diseases like diabetes has been well-studied. Metformin, a medication commonly used for type 2 diabetes, has shown potential disease-modifying effects on various aspects of AD pathophysiology.
BIOCHEMICAL PHARMACOLOGY
(2022)
Article
Clinical Neurology
Guilian Xu, Brittany S. Ulm, John Howard, Susan E. Fromholt, Qing Lu, Brian Benedict Lee, Ariel Walker, David R. Borchelt, Jada Lewis
Summary: The study aims to investigate the pathological interaction between amyloidosis and tauopathy in Alzheimer's disease, and found that the development of tauopathy is exacerbated by the presence of newly forming amyloid deposits in younger brains and mature deposits in older brains.
NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Long Wang, Xindong Shui, Yingxue Mei, Yongfang Xia, Guihua Lan, Li Hu, Mi Zhang, Chen-Ling Gan, Ruomeng Li, Yuan Tian, Quling Wang, Xi Gu, Dongmei Chen, Tao Zhang, Tae Ho Lee
Summary: This study identified miR-143-3p as a potential candidate for targeting DAPK1 in Alzheimer's disease. miR-143-3p inhibited the translation of DAPK1 and reduced tau phosphorylation, while promoting neurite outgrowth and microtubule assembly. It also decreased amyloid precursor protein phosphorylation and the generation of Aβ. Furthermore, miR-143-3p levels were downregulated and inversely correlated with DAPK1 expression in the hippocampus of AD patients.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Neurosciences
Biao Luo, Jian Chen, Gui-Feng Zhou, Xiao-Yong Xie, Jing Tang, Qi-Xin Wen, Li Song, Shi-Qi Xie, Yan Long, Guo-Jun Chen, Xiao-Tong Hu
Summary: Apicidin improves AD symptoms in APP/PS1 mice by regulating the expression of ADAM10, leading to a decrease in A beta levels rather than phosphorylation of tau.
CNS NEUROSCIENCE & THERAPEUTICS
(2023)
Article
Biochemistry & Molecular Biology
Laura Schnoeder, Wenqiang Quan, Ye Yu, Inge Tomic, Qinghua Luo, Wenlin Hao, Guoping Peng, Dong Li, Klaus Fassbender, Yang Liu
Summary: In the brains of Alzheimer's disease (AD) mice, deficiency of IKK beta in neurons reduces levels of amyloid-beta-peptide (Aβ) and phosphorylated tau (p-tau), modifies inflammatory activation, and improves cognitive function. The deficiency also decreases BACE1 protein and activity, increases expression of PP2A isoform A, and enhances autophagy. However, the protective effects of IKK beta deficiency differ in APP and tau-transgenic mice. Further studies are needed to understand the interaction between Aβ and p-tau before targeting IKK beta/NF-kappa B for AD therapies.
Article
Clinical Neurology
Yalun Zhang, Yi Zhang, Yahyah Aman, Cheung Toa Ng, Wing-Hin Chau, Zhigang Zhang, Ming Yue, Christopher Bohm, Yizhen Jia, Siwen Li, Qiuju Yuan, Jennifer Griffin, Kin Chiu, Dana S. M. Wong, Binbin Wang, Dongyan Jin, Ekaterina Rogaeva, Paul E. Fraser, Evandro F. Fang, Peter St George-Hyslop, You-Qiang Song
Summary: Research has shown that the transcription factor PAX6 is increased in Alzheimer's disease, playing a key role in the hyperphosphorylation of tau protein induced by amyloid-beta. Downregulation of PAX6 can protect against amyloid-beta-induced neuronal death. This study provides novel potential targets for pharmaceutical intervention by modulating signaling pathways involving CDK/pRB/E2F1.
Article
Chemistry, Medicinal
Li Gao, Dongqing Wang, Jia Ren, Xue Tan, Jiayuan Chen, Zheng Kong, Yunan Nie, Ming Yan
Summary: This study revealed that acteoside (AS) has beneficial effects on cognitive function and anxious behaviors in Alzheimer's disease (AD). AS promotes Aβ degradation, inhibits tau hyperphosphorylation, and reduces the activity of GSK3β.
PHYTOTHERAPY RESEARCH
(2023)
Article
Biochemistry & Molecular Biology
Yuki Kobayashi, Shogo Kohbuchi, Noriko Koganezawa, Yuko Sekino, Tomoaki Shirao, Takaomi C. Saido, Takashi Saito, Yumiko Saito
Summary: The primary cilium, a sensory organelle extending from cell bodies, plays a crucial role in neuronal integrity and connectivity. Research suggests a potential link between the structural alterations of neuronal cilia and the development of Alzheimer's disease and ciliopathies, which are characterized by memory and cognitive impairments.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(2022)
Article
Cell Biology
Na Li, Ning Bai, Xiong Zhao, Rong Cheng, Xuan Wu, Bo Jiang, Xiaoman Li, Mingli Xue, Hongde Xu, Qiqiang Guo, Wendong Guo, Mengtao Ma, Sunrun Cao, Yanling Feng, Xiaoyu Song, Zhuo Wang, Xiaoyu Zhang, Yu Zou, Difei Wang, Hua Liu, Liu Cao
Summary: Alzheimer's disease (AD) is an age-related neurodegenerative disorder characterized by amyloid-beta (Aβ) deposition and neurofibrillary tangles. The ratio of SIRT2:SIRT1 is elevated in aging mice and AD mouse models, and SIRT1 overexpression prevents Aβ-induced neurotoxicity. SIRT1 inhibits the binding of SIRT2 to APP, thus reducing amyloidogenic processing of APP and providing a potential avenue for therapeutic intervention of AD.
Article
Biochemistry & Molecular Biology
Paige Grant, Jitendra Kumar, Satyabrata Kar, Michael Overduin
Summary: The study investigated the effects of two specific kinase inhibitors for CaMK1D on A beta-mediated toxicity in mouse primary cortical neurons. While these inhibitors were able to prevent A beta-induced tau hyperphosphorylation, they were not able to protect cells from A beta induced toxicity. Further research and development may lead to the potential use of these inhibitors as part of a multi-drug strategy to combat Alzheimer's disease.
Review
Neurosciences
Md. Tanvir Kabir, Md. Sahab Uddin, Sonia Zaman, Yesmin Begum, Ghulam Md Ashraf, May N. Bin-Jumah, Simona G. Bungau, Shaker A. Mousa, Mohamed M. Abdel-Daim
Summary: Research indicates that neurodegenerative diseases like AD are associated with biometal imbalance and toxic metal accumulation, leading to neurotoxic activities and cell death. Aberrant expression of endogenous proteins related to metal transport is linked to AD pathogenesis.
MOLECULAR NEUROBIOLOGY
(2021)