mTOR inhibition alleviated tau phosphorylation-induced mitochondrial impairment, oxidative stress, and cognitive impairment DOI Creative Commons
Zhi Tang, Min Guo,

Yuanting Ding

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Ноя. 24, 2024

Aim: Hyperphosphorylated tau plays a crucial role in the pathogenesis of Alzheimer's disease (AD). Whether mammalian target rapamycin (mTOR) directly interacts with Tau protein at Ser214, Ser356 and Thr231 is not clear. This study aimed to investigate whether mTOR-regulated phosphorylation disrupts mitochondrial dynamics function rapamycin, an mTOR inhibitor, can modulate levels attenuate AD-related alterations. Methods: Adeno-associated virus (AAV) vectors were used intracranially deliver TauS214E/T231E/S356E (Tau3E) variant into 2-month-old C57BL/6 mice. The mice intraperitoneally administered inhibitor for one week, followed by assessment via Morris water maze test. Western blot analysis, immunofluorescence staining, flow cytometry employed measure expression mTOR, p70S6K, tau; dynamics; reactive oxygen species (ROS) HT22 cells mouse model overexpressing Tau3E, as well postmortem brain tissues from AD patients. Results: p-mTORS2448 colocalized p-TauSer214, p-TauSer356, p-TauThr231 hippocampal CA3 region Tau3E presented elevated p-mTOR, downstream p-p70S6K, ROS production; fragmentation; p-TauThr231. Rapamycin treatment partially mitigated cognitive molecular alterations Conclusion: revealed causal link between Ser356, p-Thr231 upregulation impairments ROS, dysfunction function. Treatment using (i.p.) alleviate impairment, reduce p-Tau restore homeostasis, neuronal loss impairment

Язык: Английский

Increased Cerebral Level of P2X7R in a Tauopathy Mouse Model by PET Using [18F]GSK1482160 DOI Creative Commons
Yanyan Kong, Lei Cao, Jiao Wang

и другие.

ACS Chemical Neuroscience, Год журнала: 2024, Номер 15(11), С. 2112 - 2120

Опубликована: Май 22, 2024

Neuroinflammation plays an important role in Alzheimer's disease and primary tauopathies. The aim of the current study was to map [18F]GSK1482160 for imaging purinergic P2X7R tauopathy mouse models. Small animal PET performed using widely used models (APP/PS1, 5×FAD, 3×Tg), 4-repeat (rTg4510) mice, age-matched wild-type mice. Increased uptake observed brains 7-month-old rTg4510 mice compared 3-month-old A positive correlation between hippocampal tau [18F]APN-1607 found No significant differences APP/PS1 5×FAD or 3×Tg Immunofluorescence staining further indicated distribution P2X7Rs with accumulation inclusion. These findings provide vivo evidence increased level

Язык: Английский

Процитировано

3

Hippocampal purinergic P2X7 receptor level is increased in Alzheimer’s disease patients, and associated with amyloid and tau pathologies DOI Creative Commons

Cinzia Maschio,

Junlong Wang, Upasana Maheshwari

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Фев. 28, 2024

Abstract INTRODUCTION The purinergic receptor P2X7R, which is expressed on microglia and astrocytes, plays an important role in Alzheimer’s disease (AD). We aimed to characterize the alterations P2X7R expression AD patients by APOE ε4 allele, age sex, as well its association with amyloid tau pathology. METHODS staining quantitative analysis of amyloid, tau, astrocytes were performed postmortem hippocampal tissues from 35 patients; 31 nondemented controls; caudate/putamen tissue corticobasal degeneration (CBD), progressive supranuclear palsy (PSP) bran aged 3×Tg mouse model AD. RESULTS Activated reactive observed hippocampi exhibited altered morphology denser cells pronounced ramifications. Hippocampal intensity was greater subfields than those controls correlated level Braak stage not affected APOEε4 or age. increased around Aβ plaques, cerebral angiopathy, inclusions hippocampus CBD PSP patients. DISCUSSION found compared non-demented control, pathologies. a potential marker for neuroinflammation

Язык: Английский

Процитировано

1

Increased regional P2X7R uptake detected by [18F]GSK1482160 PET in a tauopathy mouse model DOI Creative Commons
Yanyan Kong, Lei Cao, Jiao Wang

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Янв. 28, 2024

Abstract Neuroinflammation plays an important role in Alzheimer’s disease and primary tauopathies. The aim of the current study was to map [ 18 F]GSK1482160 for imaging purinergic P2X7R tauopathy mouse models. MicroPET performed using widely used models (APP/PS1, 5×FAD 3×Tg), 4-repeat (rTg4510) mice age-matched wild-type mice. Increased uptake observed cortex basal forebrain 7-month-old rTg4510 compared 3-month-old Nonparametric Spearman’s rank analysis revealed a positive correlation between tau F]APN-1607 hippocampus No significant differences were APP/PS1 (5, 10 months), (3, 7 months) or 3×Tg (10 months). Immunofluorescence staining further indicated distribution P2X7Rs brains with accumulation inclusion These findings provide vivo evidence increased model

Язык: Английский

Процитировано

0

mTOR inhibition alleviated tau phosphorylation-induced mitochondrial impairment, oxidative stress, and cognitive impairment DOI Creative Commons
Zhi Tang, Min Guo,

Yuanting Ding

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Ноя. 24, 2024

Aim: Hyperphosphorylated tau plays a crucial role in the pathogenesis of Alzheimer's disease (AD). Whether mammalian target rapamycin (mTOR) directly interacts with Tau protein at Ser214, Ser356 and Thr231 is not clear. This study aimed to investigate whether mTOR-regulated phosphorylation disrupts mitochondrial dynamics function rapamycin, an mTOR inhibitor, can modulate levels attenuate AD-related alterations. Methods: Adeno-associated virus (AAV) vectors were used intracranially deliver TauS214E/T231E/S356E (Tau3E) variant into 2-month-old C57BL/6 mice. The mice intraperitoneally administered inhibitor for one week, followed by assessment via Morris water maze test. Western blot analysis, immunofluorescence staining, flow cytometry employed measure expression mTOR, p70S6K, tau; dynamics; reactive oxygen species (ROS) HT22 cells mouse model overexpressing Tau3E, as well postmortem brain tissues from AD patients. Results: p-mTORS2448 colocalized p-TauSer214, p-TauSer356, p-TauThr231 hippocampal CA3 region Tau3E presented elevated p-mTOR, downstream p-p70S6K, ROS production; fragmentation; p-TauThr231. Rapamycin treatment partially mitigated cognitive molecular alterations Conclusion: revealed causal link between Ser356, p-Thr231 upregulation impairments ROS, dysfunction function. Treatment using (i.p.) alleviate impairment, reduce p-Tau restore homeostasis, neuronal loss impairment

Язык: Английский

Процитировано

0