Intracellular and extracelluar cyclic GMP in the brain and the hippocampus

Taoro‐González, Lucas; Cabrera‐Pastor, Andrea; Sancho-Alonso, María; Felipo, Vicente

doi:10.1016/bs.vh.2021.11.006

Cited by 3 publications

(1 citation statement)

References 160 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Studies have shown that decreased H3 and H4 acetylation results in decreased neurotrophic factor expression and increased deposition of amyloid β (Aβ) plaques, neurofibrillary tangles, and Lewy bodies in Alzheimer's disease (AD) and Parkinson's disease (PD) [6]. Overload of Aβ in AD causes disruption in alpha-amino-3-hydroxy-5methylisoxazole-4-propionic acid subtype glutamate receptor (AMPAR) trafficking and subsequent deficits in long-term potentiation (LTP) [8]. AMPARs belong to a class of glutamate receptors that are widely present in neurons and glial cells and are important in the regulation of synaptic plasticity [9].…”

Section: Introductionmentioning

confidence: 99%

Connecting the ends: signaling via receptor tyrosine kinases and cytoskeletal degradation in neurodegeneration

Sengupta,

Das,

Majumder

et al. 2024

Explor Neurosci

View full text Add to dashboard Cite

Receptor tyrosine kinases (RTKs) are known to perform versatile roles in disease landscapes, which determine the fate of the cell. Although much has been discussed from the perspective of proliferation, this review focuses on the impact of RTK-mediated signaling and its role in cytoskeletal degradation, the penultimate stage of cellular degeneration. In the case of degenerative diseases such as Alzheimer’s disease (AD), Huntington’s disease (HD), amyotrophic lateral sclerosis (ALS), Parkinson’s disease (PD), age-related macular degeneration (AMD), and type 2 diabetes mellitus (T2DM), RTK signaling has been reported to be perturbed in several studies. The implications of downstream signaling via these receptors through canonical and noncanonical pathways alter the status of actin filaments that provide structural integrity to cells. Degenerative signaling leads to the altered status of rat sarcoma (Ras), Ras homologous (Rho), Ras-related C3 botulinum toxin substrate (Rac), and cell division control protein 42 (Cdc42), the best-characterized components of the cytoskeleton remodeling machinery. RTKs, along with their diverse adaptor partners and other membrane receptors, affect the functionality of Rho family guanosine triphosphate hydrolases (GTPases), which are discussed in this review. To conclude, this review focuses on therapeutic strategies targeting RTKs and Rho GTPase-mediated pathways that can be more effective due to their combined multifactorial impact on neurodegenerative cascades.

show abstract

Section: Introductionmentioning

confidence: 99%