Rock inhibitors in Alzheimer’s disease
Alzheimer’s disease (AD) is the most common age-related neurodegenerative disease and cause of dementia. AD pathology primarily involves the formation of amyloid β (Aβ) plaques and neurofibrillary tangles containing hyperphosphorylated tau (p-tau). While Aβ targeted treatments have shown clinical pr...
Saved in:
| Main Authors: | , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Frontiers Media S.A.
2025-03-01
|
| Series: | Frontiers in Aging |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/articles/10.3389/fragi.2025.1547883/full |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1850059847168425984 |
|---|---|
| author | Chao Zheng Chao Zheng Weiming Xia Weiming Xia Weiming Xia Jianhua Zhang |
| author_facet | Chao Zheng Chao Zheng Weiming Xia Weiming Xia Weiming Xia Jianhua Zhang |
| author_sort | Chao Zheng |
| collection | DOAJ |
| description | Alzheimer’s disease (AD) is the most common age-related neurodegenerative disease and cause of dementia. AD pathology primarily involves the formation of amyloid β (Aβ) plaques and neurofibrillary tangles containing hyperphosphorylated tau (p-tau). While Aβ targeted treatments have shown clinical promise, other aspects of AD pathology such as microgliosis, astrocytosis, synaptic loss, and hypometabolism may be viable targets for treatment. Among notable novel therapeutic approaches, the Ras homolog (Rho)-associated kinases (ROCKs) are being investigated as targets for AD treatment, based on the observations that ROCK1/2 levels are elevated in AD, and activation or inhibition of ROCKs changes dendritic/synaptic structures, protein aggregate accumulation, inflammation, and gliosis. This review will highlight key findings on the effects of ROCK inhibition in Aβ and ptau pathologies, as well as its effects on neuroinflammation, synaptic density, and potentially metabolism and bioenergetics. |
| format | Article |
| id | doaj-art-3eeb91e26d8845e6995ce18c35c4de0e |
| institution | DOAJ |
| issn | 2673-6217 |
| language | English |
| publishDate | 2025-03-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Aging |
| spelling | doaj-art-3eeb91e26d8845e6995ce18c35c4de0e2025-08-20T02:50:45ZengFrontiers Media S.A.Frontiers in Aging2673-62172025-03-01610.3389/fragi.2025.15478831547883Rock inhibitors in Alzheimer’s diseaseChao Zheng0Chao Zheng1Weiming Xia2Weiming Xia3Weiming Xia4Jianhua Zhang5Azrieli Centre for Neuro-Radiochemistry, Brain Health Imaging Centre, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health (CAMH), Toronto, ON, CanadaDepartments of Psychiatry, Chemistry, Pharmacology and Toxicology, University of Toronto, Toronto, ON, CanadaGeriatric Research Education and Clinical Center, Bedford VA Healthcare System, Bedford, MA, United StatesDepartment of Pharmacology, Physiology and Biophysics, Boston University Chobanian and Avedisian School of Medicine, Boston, MA, United StatesDepartment of Biological Sciences, University of Massachusetts Kennedy College of Science, Lowell, MA, United StatesDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL, United StatesAlzheimer’s disease (AD) is the most common age-related neurodegenerative disease and cause of dementia. AD pathology primarily involves the formation of amyloid β (Aβ) plaques and neurofibrillary tangles containing hyperphosphorylated tau (p-tau). While Aβ targeted treatments have shown clinical promise, other aspects of AD pathology such as microgliosis, astrocytosis, synaptic loss, and hypometabolism may be viable targets for treatment. Among notable novel therapeutic approaches, the Ras homolog (Rho)-associated kinases (ROCKs) are being investigated as targets for AD treatment, based on the observations that ROCK1/2 levels are elevated in AD, and activation or inhibition of ROCKs changes dendritic/synaptic structures, protein aggregate accumulation, inflammation, and gliosis. This review will highlight key findings on the effects of ROCK inhibition in Aβ and ptau pathologies, as well as its effects on neuroinflammation, synaptic density, and potentially metabolism and bioenergetics.https://www.frontiersin.org/articles/10.3389/fragi.2025.1547883/fullAlzheimer’s diseasefasudilamyloidphosphorylated tauglucose metabolismPET imaging |
| spellingShingle | Chao Zheng Chao Zheng Weiming Xia Weiming Xia Weiming Xia Jianhua Zhang Rock inhibitors in Alzheimer’s disease Frontiers in Aging Alzheimer’s disease fasudil amyloid phosphorylated tau glucose metabolism PET imaging |
| title | Rock inhibitors in Alzheimer’s disease |
| title_full | Rock inhibitors in Alzheimer’s disease |
| title_fullStr | Rock inhibitors in Alzheimer’s disease |
| title_full_unstemmed | Rock inhibitors in Alzheimer’s disease |
| title_short | Rock inhibitors in Alzheimer’s disease |
| title_sort | rock inhibitors in alzheimer s disease |
| topic | Alzheimer’s disease fasudil amyloid phosphorylated tau glucose metabolism PET imaging |
| url | https://www.frontiersin.org/articles/10.3389/fragi.2025.1547883/full |
| work_keys_str_mv | AT chaozheng rockinhibitorsinalzheimersdisease AT chaozheng rockinhibitorsinalzheimersdisease AT weimingxia rockinhibitorsinalzheimersdisease AT weimingxia rockinhibitorsinalzheimersdisease AT weimingxia rockinhibitorsinalzheimersdisease AT jianhuazhang rockinhibitorsinalzheimersdisease |