Aug 2026· InflammoPharmacology· Vol 34, pp. 6059 - 6088· 0 citations· 212 references
Medicine
TL;DR
Overall, this review makes a case for integrative, pathway-based therapeutic models, and multiple approaches may facilitate for drug development, biomarker identification and patient management in Alzheimer's disease.
This work aimed to identify AD-related olfactory and visual or retinal abnormalities, combine core inflammatory pathways and their interactions with amyloid-β and tau pathology, and summarize actionable targets and candidate interventions along a “receptor–intracellular signaling-inflammasome-effector” axis, to inform...
Yanjiao Xu, Guimei Zhang, Xinran Cui et al.· Frontiers in Aging Neuroscie...· 0 citations
The dual and stage‐dependent roles of microglia and astrocytes are explored, discussion of blood–brain barrier dysfunction and peripheral immune infiltration as underappreciated pathogenic contributors are expanded, and emerging evidence linking neuroinflammation specifically to tau pathology is integrated.
S. Papelian· International Journal of Dev...· 0 citations
The alterations in glucose metabolism and mitochondrial metabolism in neurons, astrocytes and microglia in AD and their relationship with neuroinflammation are summarized, while also discussing some unaddressed questions, outlining therapeutic strategies, and future promising directions.
Yinuo Lei, Liyang Liu, Yi Tang· Ageing Research Reviews· 0 citations
Neurodegenerative diseases are a heterogeneous group of chronic and progressive disorders, which are characterized by selective neuronal destruction, synaptic malfunction and progressive cognitive and locomotor dysfunction. The major ones are Alzheimer disease, Parkinson disease, Huntington disease, and amyotrophic lat...
Nisha, Sumairah Qadir· Current Pharmaceutical Resea...· 0 citations
New knowledge about the protective and detrimental aspects of neuroinflammation in AD and PD is summarized, providing an analysis on these developing prospects for targeted interventions toward slowing or stopping neurodegeneration.
R. Kumar, Kamaljeet, Sourabh Kosey· InflammoPharmacology· 0 citations
It is illustrated how endogenous pathological triggers, such as amyloid-β (Aβ) peptide, hyperphosphorylated tau, and α-synuclein, activate glial cells, contributing to chronic neuroinflammation that exacerbates neurodegeneration.
