Tau 4R Antibody,StressMarq Biosciences Inc.,SPC-815D

Tau 4R spliceoforms, generated through alternative splicing of MAPT exon 10, play a central role in the molecular pathogenesis of several primary tauopathies, including frontotemporal lobar degeneration (FTLD), corticobasal degeneration (CBD), and progressive supranuclear palsy (PSP). An imbalance in the physiological 3R:4R tau ratio disrupts microtubule stabilization and accelerates the formation of pathogenic tau aggregates, underscoring the importance of spliceoform homeostasis in maintaining neuronal integrity. Elevated expression of 4R tau, particularly in disease contexts such as VCP-related FTD, has been shown to drive neurodegeneration by promoting tau hyperphosphorylation, endolysosomal dysfunction, and apoptosis, demonstrating a direct causal link between increased 4R tau burden and neuronal vulnerability. Moreover, emerging evidence emphasizes that tau isoform imbalance is itself a pathogenic driver across multiple neurodegenerative diseases, with 4R-dominant states contributing to disease-specific patterns of tau aggregation and clinical progression, further highlighting the need for mechanistic and therapeutic focus on 4R spliceoform regulation.

Neurofibrillary tangle protein, paired helical filament‑tau, PHF‑tau, MAPTL, MTBT1, TAU, TAU‑D (4R isoform), 4R Tau, 4‑repeat MAPT isoform, Tau 4R2N