Alzheimer's disease (AD) is the most common type of
dementia worldwide, characterized by the deposition of neurofibrillary tangles and
amyloid-β (Aβ)
peptides in the brain. Additionally, increasing evidence demonstrates that a neuroinflammatory state and oxidative stress,
iron-dependent, play a crucial role in the onset and
disease progression. Besides conventional
therapies, the use of natural-based products represents a future medical option for AD treatment and/or prevention. We, therefore, evaluated the effects of a
ribonucleotides-based ingredient (Ribodiet®) in a non-genetic mouse model of AD. To this aim, mice were injected intracerebroventricularly (i.c.v.) with Aβ1-42
peptide (3 µg/3 μl) and after with Ribodiet® (0.1-10 mg/mouse) orally (p.o.) 3 times weekly for 21 days following the induction of experimental AD. The mnemonic and
cognitive decline was then evaluated, and, successively, we have assessed ex vivo the modulation of different cyto-
chemokines on mice brain homogenates. Finally, the level of GFAP, S100β, and
iron-related metabolic
proteins were monitored as markers of reactive
gliosis, neuro-
inflammation, and oxidative stress. Results indicate that Ribodiet® lessens oxidative stress,
brain inflammation, and
amyloid pathology via modulation of
iron-related metabolic
proteins paving the way for its rationale use for the treatment of AD and other age-related diseases.