| Autor: |
Tamagno E; Department of Neuroscience, University of Torino, Via Cherasco 15, 10126 Torino, Italy.; Neuroscience Institute of Cavalieri Ottolenghi Foundation (NICO), University of Torino, Regione Gonzole 10, Orbassano, 10043 Torino, Italy., Guglielmotto M; Department of Neuroscience, University of Torino, Via Cherasco 15, 10126 Torino, Italy.; Neuroscience Institute of Cavalieri Ottolenghi Foundation (NICO), University of Torino, Regione Gonzole 10, Orbassano, 10043 Torino, Italy., Vasciaveo V; Department of Neuroscience, University of Torino, Via Cherasco 15, 10126 Torino, Italy.; Neuroscience Institute of Cavalieri Ottolenghi Foundation (NICO), University of Torino, Regione Gonzole 10, Orbassano, 10043 Torino, Italy., Tabaton M; Unit of Geriatric Medicine, Department of Internal Medicine and Medical Specialties (DIMI), University of Genova, Viale Benedetto XV 6, 16132 Genova, Italy. |
| Abstrakt: |
The pathogenesis of Alzheimer's disease involves β amyloid (Aβ) accumulation known to induce synaptic dysfunction and neurodegeneration. The brain's vulnerability to oxidative stress (OS) is considered a crucial detrimental factor in Alzheimer's disease. OS and Aβ are linked to each other because Aβ induces OS, and OS increases the Aβ deposition. Thus, the answer to the question "which comes first: the chicken or the egg?" remains extremely difficult. In any case, the evidence for the primary occurrence of oxidative stress in AD is attractive. Thus, evidence indicates that a long period of gradual oxidative damage accumulation precedes and results in the appearance of clinical and pathological AD symptoms, including Aβ deposition, neurofibrillary tangle formation, metabolic dysfunction, and cognitive decline. Moreover, oxidative stress plays a crucial role in the pathogenesis of many risk factors for AD. Alzheimer's disease begins many years before its symptoms, and antioxidant treatment can be an important therapeutic target for attacking the disease. |
