Article
Biochemistry & Molecular Biology
Yi-An Chen, Cheng-Hsiu Lu, Chien-Chih Ke, Sain-Jhih Chiu, Chi-Wei Chang, Bang-Hung Yang, Jun G. Gelovani, Ren-Shyan Liu
Summary: The study revealed an association between class IIa HDACs and A beta, therapeutic benefits of a selective HDAC4 inhibitor, and the potential of using [F-18]TFAHA as an epigenetic radiotracer for AD, which could aid in the development of AD-related neuroimaging approaches and therapies.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
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)
Review
Biochemistry & Molecular Biology
Filippa Lo Cascio, Paola Marzullo, Rakez Kayed, Antonio Palumbo Piccionello
Summary: This review highlights recent research on modifying the structure of curcumin to search for new effective therapeutic agents against neurodegenerative diseases, with a particular focus on Alzheimer's disease.
Article
Clinical Neurology
Batbayar Tumurbaatar, Anna Fracassi, Pietro Scaduto, Jutatip Guptarak, Randall Woltjer, Daniel Jupiter, Giulio Taglialatela
Summary: This study investigates the association of autophagy with cognitive integrity in individuals with Alzheimer's disease neuropathology but without dementia. The results suggest that preserved autophagy may protect against cognitive decline in these individuals.
ALZHEIMERS & DEMENTIA
(2023)
Article
Neurosciences
Keiko Takasu, Kazuki Niidome, Minoru Hasegawa, Koichi Ogawa
Summary: This study revealed that histone acetylation regulates hippocampal gamma oscillations by modulating the activity of fast spiking interneurons, and the deficits in gamma oscillations in AD model mice can be restored by HDAC inhibitor or NR4a activator. These findings suggest a potential therapeutic target for treating cognitive impairment in AD patients.
FRONTIERS IN MOLECULAR NEUROSCIENCE
(2021)
Review
Biochemistry & Molecular Biology
Tadanori Hamano, Soichi Enomoto, Norimichi Shirafuji, Masamichi Ikawa, Osamu Yamamura, Shu-Hui Yen, Yasunari Nakamoto
Summary: Neurofibrillary tangles and senile plaques are pathological hallmarks of Alzheimer's disease, with autophagy disturbances being implicated in tau protein accumulation. Therapeutic strategies focusing on autophagic modulation may hold promise in AD treatment.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Cell Biology
Xing Jun Jiang, Yan Qing Wu, Rong Ma, Yan Min Chang, Lu Lu Li, Jia Hui Zhu, Gong Ping Liu, Gang Li
Summary: This study found that overexpression of PINK1 can promote the degradation of accumulated tau proteins in patients with AD, improving cognitive abilities and rescuing damaged neurons and synapses. Furthermore, PINK1 also improves mitochondrial dysfunction caused by tau proteins. This suggests that PINK1 may be a potential target for AD treatment.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2022)
Article
Neurosciences
Joseph R. Winer, Allison Morehouse, Laura Fenton, Theresa M. Harrison, Lylian Ayangma, Mark Reed, Samika Kumar, Suzanne L. Baker, William J. Jagust, Matthew P. Walker
Summary: This study found that early-stage tau and Aβ deposition in Alzheimer's disease can impact sleep, with tau burden leading to worse objective sleep and Aβ burden associated with decreased self-reported sleep quality. Aβ deposition also predicts a mismatch between objective and subjective sleep evaluation, with individuals underestimating their sleep, which is further linked to worse executive function.
JOURNAL OF NEUROSCIENCE
(2021)
Article
Clinical Neurology
Amelia Strom, Leonardo Iaccarino, Lauren Edwards, Orit H. Lesman-Segev, David N. Soleimani-Meigooni, Julie Pham, Suzanne L. Baker, Susan M. Landau, William J. Jagust, Bruce L. Miller, Howard J. Rosen, Maria Luisa Gorno-Tempini, Gil D. Rabinovici, Renaud La Joie
Summary: Posterior cortical hypometabolism measured with F-18-fluorodeoxyglucose (FDG)-PET is a marker of neurodegeneration in Alzheimer's disease, and it is mainly associated with structural neurodegeneration and tau pathology, rather than amyloid pathology.
Review
Biochemistry & Molecular Biology
Yuanxin Zhao, Buhan Liu, Jian Wang, Long Xu, Sihang Yu, Jiaying Fu, Xiaoyu Yan, Jing Su
Summary: Neuroinflammation mediated by microglia is a common feature in neurodegenerative diseases. The accumulation of Aβ and tau proteins can disrupt the metabolism of microglia, leading to neuroinflammation.
Article
Multidisciplinary Sciences
Yin Xu, Nicholas E. Propson, Shuqi Du, Wen Xiong, Hui Zheng
Summary: Studies indicate that microglial-specific autophagy, represented by Atg7, plays a crucial role in regulating lipid metabolism and neuroinflammation. Deletion of Atg7 in microglia leads to a proinflammatory status and exacerbates intraneuronal tau pathology.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
(2021)
Article
Immunology
Mahdieh Mehrpouri, Atieh Pourbagheri-Sigaroodi, Davood Bashash
Summary: This article outlines the role of epigenetic modulations, particularly histone deacetylases, in hematologic malignancies and their therapeutic potential. Research suggests that HDACs play a significant role in hematopoiesis and the development of blood cancers.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2021)
Review
Medicine, General & Internal
Lorenz Gerbeth, Rainer Glauben
Summary: Inflammatory bowel diseases are severe conditions of the gastrointestinal tract associated with defects in epithelial cell function. Current therapeutic approaches focus on targeting immune cell signaling to alleviate symptoms. The protein family of histone deacetylases (HDACs) has gained attention as potential therapeutic targets for these conditions.
FRONTIERS IN MEDICINE
(2021)
Review
Neurosciences
Christopher Daniel Morrone, Radha Raghuraman, S. Abid Hussaini, Wai Haung Yu
Summary: Failed proteostasis, reduced protein degradation and clearance, is a well-documented feature in Alzheimer's disease. The contribution of failed proteostasis to neuronal circuit dysfunction and cognitive decline is an emerging concept in neurodegenerative research. This study highlights the bidirectional relationship between sleep disruption and proteostasis failure in Alzheimer's disease progression, where sleep loss impairs protein clearance and disrupted proteostasis further impairs sleep, ultimately leading to memory impairments.
MOLECULAR NEURODEGENERATION
(2023)
Article
Chemistry, Medicinal
Kai-Cheng Hsu, Jung-Chun Chu, Hui-Ju Tseng, Chia- Liu, Hao-Ching Wang, Tony Eight Lin, Hong-Sheng Lee, Ling-Wei Hsin, Andrew H-J Wang, Chien-Huang Lin, Wei-Jan Huang
Summary: The study showed that modifying the acridine ring with phenothiazine derivatives can effectively inhibit the activity of class II HDACs, with compound 4f exhibiting the strongest inhibitory effect and promoting neurite outgrowth.
EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY
(2021)