Hippocampal mGluR5 levels are comparable in Alzheimer′s and control brains, and divergently influenced by amyloid and tau in control brain DOI Creative Commons
Junlong Wang,

Serena Savodalli,

Yanyan Kong

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: May 26, 2024

Abstract Background Metabotropic glutamate receptor 5 (mGluR5) modulates excitatory glutamatergic synaptic transmission and plays an important role in learning memory formation neurodegeneration amyloid deposition Alzheimer’s disease (AD). Conflicting results on the cerebral mGluR5 levels AD have been reported based vivo postmortem studies. Here, we aimed to assess alterations hippocampal expression AD, associations between pathologies. Methods Immunofluorescence staining for was performed brain tissue from 34 patients 31 nondemented controls (NCs) aged 3×Tg arcAβ model mice of AD. Autoradiography slices using tracer [ 18 F]PSS232. Analysis different cellular source GRM5 RNA human mouse brains performed. Proteomic profiling pathway analysis were wild-type mice. Results No differences or entorhinal cortical detected NC groups. Hippocampal increased with Braak stage decreased level group. correlations amyloid, tau, Iba1/P2X7R hippocampus cases. Ex autoradiography revealed comparable F]PSS232 compared nontransgenic GO KEGG enrichment analyses that Shank3, Grm5 pathways upregulated Conclusion This study no difference NCs divergent influence tau pathologies NCs. Species observed as well at location. Graphical abstract

Language: Английский

Modulating Neuroinflammation as a Prospective Therapeutic Target in Alzheimer’s Disease DOI Creative Commons

Eunshil Lee,

Yongmin Chang

Cells, Journal Year: 2025, Volume and Issue: 14(3), P. 168 - 168

Published: Jan. 22, 2025

The recent approval of lecanemab highlights that the amyloid beta (Aβ) protein is an important pathological target in Alzheimer’s disease (AD) and further emphasizes significance neuroinflammatory pathways regulating Aβ accumulation. Indeed, accumulation triggers microglia activation, which are key mediators neuroinflammation. inflammatory responses this process can lead to neuronal damage functional decline. Microglia secrete proinflammatory cytokines accelerate death release anti-inflammatory growth factors contributing recovery protection. Thus, play a dual role neurodegeneration neuroprotection, complicating their function AD. Therefore, elucidating complex interactions between protein, microglia, neuroinflammation essential for developing new strategies treating This review investigates receptors involved activating aims enhance understanding how these processes impact AD, as well they be regulated. also analyzed studies reported existing literature ongoing clinical trials. Overall, will contribute regulatory mechanisms therapies slow progression

Language: Английский

Citations

1
Myricetin ameliorates cognitive impairment in 3×Tg Alzheimer’s disease mice by regulating oxidative stress and tau hyperphosphorylation DOI Creative Commons
Li Wang, Zhi Tang, Bo Li

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 177, P. 116963 - 116963

Published: June 17, 2024

Alzheimer's disease is characterized by abnormal β-amyloid (Aβ) plaque accumulation, tau hyperphosphorylation, reactive oxidative stress, mitochondrial dysfunction and synaptic loss. Myricetin, a dietary flavonoid, has been shown to exert neuroprotective effects in vitro vivo. Here, we aimed elucidate the mechanism pathways involved protective effect of myricetin.

Language: Английский

Citations

4
Decoding NLRP3 Inflammasome Activation in Alzheimer’s Disease: A Focus on Receptor Dynamics DOI

Ranika Maurya,

Abha Sharma,

Saba Naqvi

et al.

Molecular Neurobiology, Journal Year: 2025, Volume and Issue: unknown

Published: April 15, 2025

Language: Английский

Citations

0
Hippocampal mGluR5 levels are comparable in Alzheimer′s and control brains, and divergently influenced by amyloid and tau in control brain DOI Creative Commons
Junlong Wang,

Serena Savodalli,

Yanyan Kong

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: May 26, 2024

Abstract Background Metabotropic glutamate receptor 5 (mGluR5) modulates excitatory glutamatergic synaptic transmission and plays an important role in learning memory formation neurodegeneration amyloid deposition Alzheimer’s disease (AD). Conflicting results on the cerebral mGluR5 levels AD have been reported based vivo postmortem studies. Here, we aimed to assess alterations hippocampal expression AD, associations between pathologies. Methods Immunofluorescence staining for was performed brain tissue from 34 patients 31 nondemented controls (NCs) aged 3×Tg arcAβ model mice of AD. Autoradiography slices using tracer [ 18 F]PSS232. Analysis different cellular source GRM5 RNA human mouse brains performed. Proteomic profiling pathway analysis were wild-type mice. Results No differences or entorhinal cortical detected NC groups. Hippocampal increased with Braak stage decreased level group. correlations amyloid, tau, Iba1/P2X7R hippocampus cases. Ex autoradiography revealed comparable F]PSS232 compared nontransgenic GO KEGG enrichment analyses that Shank3, Grm5 pathways upregulated Conclusion This study no difference NCs divergent influence tau pathologies NCs. Species observed as well at location. Graphical abstract

Language: Английский

Citations

0