(P11-36-26) Exploring the Neuroprotective Effects of Nanoparticle Encapsulated Antioxidants in Ameliorating Alzheimer’s Disease Pathology: An In Vitro Approach

Objectives: Alzheimer’s disease (AD) is a neurodegenerative disorder marked by amyloid-beta (Aβ) accumulation and hyperphosphorylated tau, causing mitochondrial dysfunction, oxidative stress, neuroinflammation, and neuronal damage. Malvidin, a berry-derived anthocyanin, and N-acetyl cysteine (NAC), a cysteine precursor, have antioxidant and anti-inflammatory properties that may help mitigate AD pathology. However, poor bioavailability limits many bioactive compounds. We therefore hypothesize that nano-encapsulation of malvidin chloride and NAC could improve their delivery and effectiveness in cellular AD models.

Methods: HT22 (mouse hippocampal) cells were transfected with mutant amyloid precursor protein (mAPP) to create a cellular AD model showing mitochondrial dysfunction, oxidative stress, neuroinflammation, and synaptic impairment. After 24 h, cells were treated with varying concentrations of nano-encapsulated malvidin chloride (0.06, 0.08 and 0.1mM) or NAC (1, 5, and 10mM). Gene expression (RT-qPCR) was used to evaluate changes in mitochondrial and synaptic function, oxidative stress, and inflammation to assess neuroprotective effects.

Results: mAPP-transfected cells showed AD-like changes, including impaired mitochondrial function, synaptic dysfunction, oxidative stress, and neuroinflammation. Treatment with malvidin or NAC nanoparticles for 24h significantly improved these markers, restoring mitochondrial and synaptic function while reducing oxidative stress and inflammation, even at lower doses.

Conclusions: No cure currently exists for AD, and treatments only manage symptoms. These findings provide mechanistic insight into the therapeutic potential of malvidin and NAC, supporting future in vivo studies for AD intervention.

Funding Sources: Texas Tech University