ReviewNeurotoxicity research2021
Targeting Common Signaling Pathways for the Treatment of Stroke and Alzheimer's: a Comprehensive Review.
Review in Neurotoxicity research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed.
- Tuberostemonine ameliorates Alzheimer's disease pathology by suppression of the p38 MAPK signaling pathway.iScience · 2026Article
- Mesenchymal stem cells and secretome as modulators of neuroinflammation in neurological disorders.Journal of translational medicine · 2026Review
- Autophagy in ischemic stroke: pathophysiology, therapeutics, and challenges ahead.Frontiers in stroke · 2026Review
- Tailoring MAPK Pathways: New Therapeutic Avenues for Treating Alzheimer's Disease.Molecular neurobiology · 2025Review
- Innovative approaches for the treatment of stroke: a recent update.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Alzheimer's Disease Protein Targets: Comprehensive Review and Future Directions.Current pharmaceutical design · 2025Review
- Neuroprotective Potential of Glycyrrhizic Acid in Ischemic Stroke: Mechanisms and Therapeutic Prospects.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Apoptosis, Autophagy, and Mitophagy Genes in the CA3 Area in an Ischemic Model of Alzheimer's Disease with 2-Year Survival.Journal of Alzheimer's disease : JAD · 2024Article
- Alpha-, Beta-, and Gamma-Secretase, Amyloid Precursor Protein, and Tau Protein Genes in the Hippocampal CA3 Subfield in an Ischemic Model of Alzheimer's Disease with Survival up to 2 Years.Journal of Alzheimer's disease : JAD · 2024Article
- A Look at the Etiology of Alzheimer's Disease based on the Brain Ischemia Model.Current Alzheimer research · 2024Review
- Article
- Common Signaling Pathways Involved in Alzheimer's Disease and Stroke: Two Faces of the Same Coin.Journal of Alzheimer's disease reports · 2023Review
- On the Common Journey of Neural Cells through Ischemic Brain Injury and Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Yi-Zhi-Fang-Dai Formula Exerts Neuroprotective Effects Against Pyroptosis and Blood-Brain Barrier-Glymphatic Dysfunctions to Prevent Amyloid-Beta Acute Accumulation After Cerebral Ischemia and Reperfusion in Rats.Frontiers in pharmacology · 2021Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurodegenerative diseases such as stroke and Alzheimer's disease (AD) are two inter-related disorders that affect the neurons in the brain and central nervous system. Alzheimer's is a disease by undefined origin and causes. Stroke and its most common type, ischemic stroke (IS), occurs due to the blockade of cerebral blood vessels. As an important feature, both of disorders are associated with irreversible damages to the brain and nervous system. In this regard, finding common signaling pathways and the same molecular origin between these two diseases may be a promising way for their solution. On the basis of literature appraisal, the most common signaling cascades implicated in the pathogenesis of AD and stroke including notch, autophagy, inflammatory, and insulin signaling pathways were reviewed. Furthermore, current therapeutic strategies including natural and synthetic pharmaceuticals aiming modulation of respective signaling factors were scrutinized to ameliorate neural deficits in AD and stroke. Taken together, digging deeper in the common connections and signal targeting can be greatly helpful in understanding and unified treating of these disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.