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KINE-PD-28, AN ULTRA-SHORT PEPTIDE, RESCUES COGNITIVE AND SYNAPTIC DEFICITS THROUGH MICROGLIAL IMMUNE ACTIVATION AND ATTENUATION OF AMYLOID PATHOLOGY AND NEUROINFLAMMATION
Hye-Lim Chaand 3 co-authors
Kine Sciences
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS03-08AM-129
Presentation
Date TBA
Board: PS03-08AM-129
Event Information
Poster Board
PS03-08AM-129
Poster
View posterAbstract
Alzheimer’s disease (AD) is the most prevalent form of dementia, characterized by the pathological accumulation of amyloid-beta (Aβ) and hyperphosphorylated tau proteins. Despite decades of research, effective disease-modifying therapies (DMTs) remain limited due to the heterogenetic etiology and complex interplay between molecular pathology and immune dysregulation.
We present KINE-PD-28, a novel nonameric peptide that modulates microglial immunity, as a promising therapeutic candidate for AD. KINE-PD-28 suppresses disease-associated microglia (DAM, or M1-like) that are causing notorious neuroinflammation in AD and promotes anti-inflammatory (M2-like) microglial phenotypes. In the meantime, KINE-PD-28 reduced pathological Aβ accumulation through enhancing the phagocytic function of microglia. Consequently, we found that KINE-PD-28 improved the synaptic dysfunction in the hippocampus and mitigated cognitive impairment in 5xFAD mice at 6 months of age.
Collectively, our findings endorse KINE-PD-28 as a first-in-class peptide-based DMT candidate that modulates microglial multifunctional immunity in AD, thereby ameliorating cognitive impairment. KINE-PD-28 is poised to fulfill critical unmet needs in current AD therapy.
We present KINE-PD-28, a novel nonameric peptide that modulates microglial immunity, as a promising therapeutic candidate for AD. KINE-PD-28 suppresses disease-associated microglia (DAM, or M1-like) that are causing notorious neuroinflammation in AD and promotes anti-inflammatory (M2-like) microglial phenotypes. In the meantime, KINE-PD-28 reduced pathological Aβ accumulation through enhancing the phagocytic function of microglia. Consequently, we found that KINE-PD-28 improved the synaptic dysfunction in the hippocampus and mitigated cognitive impairment in 5xFAD mice at 6 months of age.
Collectively, our findings endorse KINE-PD-28 as a first-in-class peptide-based DMT candidate that modulates microglial multifunctional immunity in AD, thereby ameliorating cognitive impairment. KINE-PD-28 is poised to fulfill critical unmet needs in current AD therapy.
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