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6. FSH blockade improves cognition in mice with Alzheimer’s disease

Author

Xiong, Jing, Kang, Seong Su, Wang, Zhihao, Liu, Xia, Kuo, Tan-Chun, Korkmaz, Funda, Padilla, Ashley, Miyashita, Sari, Chan, Pokman, Zhang, Zhaohui, Katsel, Pavel, Burgess, Jocoll, Gumerova, Anisa, Ievleva, Kseniia, Sant, Damini, Yu, Shan-Ping, Muradova, Valeriia, Frolinger, Tal, Lizneva, Daria, Iqbal, Jameel, Goosens, Ki A., Gera, Sakshi, Rosen, Clifford J., Haroutunian, Vahram, Ryu, Vitaly, Yuen, Tony, Zaidi, Mone, and Ye, Keqiang

Published
2022
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16. Reprogramming Glioblastoma Cells into Non-Cancerous Neuronal Cells as a Novel Anti-Cancer Strategy.

Author

Jiang, Michael Q., Yu, Shan Ping, Estaba, Takira, Choi, Emily, Berglund, Ken, Gu, Xiaohuan, and Wei, Ling

Subjects
*NEURAL stem cells, *GLIOBLASTOMA multiforme, *P53 antioncogene, *BRAIN tumors, *DEVELOPMENTAL neurobiology, *NEUROLOGICAL disorders
Abstract

Glioblastoma Multiforme (GBM) is an aggressive brain tumor with a high mortality rate. Direct reprogramming of glial cells to different cell lineages, such as induced neural stem cells (iNSCs) and induced neurons (iNeurons), provides genetic tools to manipulate a cell's fate as a potential therapy for neurological diseases. NeuroD1 (ND1) is a master transcriptional factor for neurogenesis and it promotes neuronal differentiation. In the present study, we tested the hypothesis that the expression of ND1 in GBM cells can force them to differentiate toward post-mitotic neurons and halt GBM tumor progression. In cultured human GBM cell lines, including LN229, U87, and U373 as temozolomide (TMZ)-sensitive and T98G as TMZ-resistant cells, the neuronal lineage conversion was induced by an adeno-associated virus (AAV) package carrying ND1. Twenty-one days after AAV-ND1 transduction, ND1-expressing cells displayed neuronal markers MAP2, TUJ1, and NeuN. The ND1-induced transdifferentiation was regulated by Wnt signaling and markedly enhanced under a hypoxic condition (2% O2 vs. 21% O2). ND1-expressing GBM cultures had fewer BrdU-positive proliferating cells compared to vector control cultures. Increased cell death was visualized by TUNEL staining, and reduced migrative activity was demonstrated in the wound-healing test after ND1 reprogramming in both TMZ-sensitive and -resistant GBM cells. In a striking contrast to cancer cells, converted cells expressed the anti-tumor gene p53. In an orthotopical GBM mouse model, AAV-ND1-reprogrammed U373 cells were transplanted into the fornix of the cyclosporine-immunocompromised C57BL/6 mouse brain. Compared to control GBM cell-formed tumors, cells from ND1-reprogrammed cultures formed smaller tumors and expressed neuronal markers such as TUJ1 in the brain. Thus, reprogramming using a single-factor ND1 overcame drug resistance, converting malignant cells of heterogeneous GBM cells to normal neuron-like cells in vitro and in vivo. These novel observations warrant further research using patient-derived GBM cells and patient-derived xenograft (PDX) models as a potentially effective treatment for a deadly brain cancer and likely other astrocytoma tumors. [ABSTRACT FROM AUTHOR]

Published
2024
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38. Lithium: An Old Drug for New Therapeutic Strategy for Alzheimer's Disease and Related Dementia.

Author

Shim, Seong Sool, Berglund, Ken, and Yu, Shan Ping

Subjects
ALZHEIMER'S disease, CEREBRAL amyloid angiopathy, MILD cognitive impairment, DEMENTIA, NEUROPLASTICITY
Abstract

Background: Although Alzheimer's disease (AD) is the most common form of dementia, the effective treatment of AD is not available currently. Multiple trials of drugs, which were developed based on the amyloid hypothesis of AD, have not been highly successful to improve cognitive and other symptoms in AD patients, suggesting that it is necessary to explore additional and alternative approaches for the disease-modifying treatment of AD. The diverse lines of evidence have revealed that lithium reduces amyloid and tau pathology, attenuates neuronal loss, enhances synaptic plasticity, and improves cognitive function. Clinical studies have shown that lithium reduces the risk of AD and deters the progress of mild cognitive impairment and early AD. Summary: Our recent study has revealed that lithium stabilizes disruptive calcium homeostasis, and subsequently, attenuates the downstream neuropathogenic processes of AD. Through these therapeutic actions, lithium produces therapeutic effects on AD with potential to modify the disease process. This review critically analyzed the preclinical and clinical studies for the therapeutic effects of lithium on AD. We suggest that disruptive calcium homeostasis is likely to be the early neuropathological mechanism of AD, and the stabilization of disruptive calcium homeostasis by lithium would be associated with its therapeutic effects on neuropathology and cognitive deficits in AD. Key Messages: Lithium is likely to be efficacious for AD as a disease-modifying drug by acting on multiple neuropathological targets including disruptive calcium homeostasis. [ABSTRACT FROM AUTHOR]

Published
2023
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43. Cleavage of tau by asparagine endopeptidase mediates the neurofibrillary pathology in Alzheimer's disease

Author

Zhang, Zhentao, Song, Mingke, Liu, Xia, Kang, Seong Su, Kwon, Il-Sun, Duong, Duc M., Seyfried, Nicholas T., Hu, William T., Liu, Zhixue, Wang, Jian-Zhi, Cheng, Liming, Sun, Yi.E., Yu, Shan Ping, Levey, Allan I., and Ye, Keqiang

Subjects
Asparagine -- Research, Proteases -- Research -- Analysis -- Physiological aspects, Alzheimer's disease -- Research -- Analysis, Biological sciences, Health
Abstract

Neurofibrillary tangles (NFTs), composed of truncated and hyperphosphorylated tau, are a common feature of numerous aging-related neurodegenerative diseases, including Alzheimer's disease (AD). However, the molecular mechanisms mediating tau truncation and aggregation during aging remain elusive. Here we show that asparagine endopeptidase (AEP), a lysosomal cysteine proteinase, is activated during aging and proteolytically degrades tau, abolishes its microtubule assembly function, induces tau aggregation and triggers neurodegeneration. AEP is upregulated and active during aging and is activated in human AD brain and tau P301S-transgenic mice with synaptic pathology and behavioral impairments, leading to tau truncation in NFTs. Tau P301S-transgenic mice with deletion of the gene encoding AEP show substantially reduced tau hyperphosphorylation, less synapse loss and rescue of impaired hippocampal synaptic function and cognitive deficits. Mice infected with adeno-associated virus encoding an uncleavable tau mutant showed attenuated pathological and behavioral defects compared to mice injected with adeno-associated virus encoding tau P301S. Together, these observations indicate that AEP acts as a crucial mediator of tau-related clinical and neuropathological changes. Inhibition of AEP may be therapeutically useful for treating tau-mediated neurodegenerative diseases., AD is a progressive neurodegenerative disease characterized by two neuropathological hallmarks: extracellular senile plaque deposits, composed of amyloid beta (Aβ), and intracellular NFTs, made of truncated and hyperphosphorylated tau. Tau-mediated [...]

Published
2014
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