Histological and Memory Alterations in an Innovative Alzheimer's Disease Animal Model by Vanadium Pentoxide...

Area of Science:

• Neuroscience
• Toxicology
• Pathology

Background:

• Chronic vanadium pentoxide (V2O5) exposure can induce cytoskeletal changes and neuronal cell death, suggesting a link to Alzheimer's disease (AD) pathogenesis.
• Previous research indicates V2O5 may interact with cytoskeletal proteins and inhibit tyrosine phosphatases, contributing to AD-like pathology.

Purpose of the Study:

• To characterize a novel experimental model of Alzheimer's disease (AD) using chronic V2O5 inhalation in rats.
• To assess spatial memory deficits and neurohistopathological changes, including neurofibrillary tangles (NFTs) and amyloid-β (Aβ) plaques, in an V2O5-induced AD model.

Main Methods:

• Twenty male Wistar rats were divided into control and V2O5-exposed groups, receiving V2O5 inhalation three times weekly for six months.
• Spatial memory was evaluated monthly using the T-maze test.
• Histological analyses of brain structures (frontal cortex, entorhinal cortex, CA1, subiculum, amygdala) were performed using Congo red, Bielschowsky, and Golgi staining.

Main Results:

• Rats exposed to V2O5 exhibited significant spatial memory impairment starting from the third month of exposure.
• Histopathological examination revealed neurofibrillary tangles (NFTs) and amyloid-β (Aβ) plaque accumulation in vascular endothelium and neurons.
• Dendritic spine loss and neuronal loss were observed in all analyzed brain regions, with the CA1 hippocampus being the most severely affected.

Conclusions:

• The V2O5 inhalation model effectively replicates key neurodegenerative changes characteristic of Alzheimer's disease (AD).
• This model aligns with Braak AD stage IV, indicating its suitability for testing therapeutic strategies aimed at halting neurodegeneration.