Salute
di Andrea Tognelli, Farmacista - Firenze
I mitocondri sono microscopici organelli presenti nelle cellule di tutti gli esseri viventi.
Producono la maggioranza dell’energia necessaria alle funzioni cellulari, oltre ad essere coinvolti in molteplici meccanismi necessari per il benessere del nostro organismo.
Ad aprile 2026, la rivista Neural Regeneration Research ha confermato ed approfondito le attuali conoscenze, ed valore clinico degli interventi per proteggere l’integrità dei mitocondri e, di conseguenza, la buona funzionalità cellulare e la salute generale (1).
Strategie generali per proteggere i mitocondri
Secondo la più recenti ricerche, esercizio fisico, integrazione mirata, controllo dell’apporto calorico giornaliero, digiuno intermittente ecc., sono le strategie vincenti migliorare la performance dei mitocondri, per rallentare l’invecchiamento, migliorare la performance cognitiva e ridurre il rischio di malattie croniche (1).
I mitocondri sono particolarmente sensibili agli agenti stressanti (inquinanti, raggi UV, fumo ecc.), che possono danneggiare il DNA e scatenare vari meccanismi causa di neuroinfiammazione, reazioni immunitarie e di altre alterazioni, lesive per i neuroni (1, 2, 3).
Tutto questo aumenta il rischio d’insorgenza del decadimento cognitivo ed Alzheimer (1-5); morbo di Parkinson (1-8); sclerosi laterale amiotrofica (1-10).
Si aggiungono inoltre altri fenomeni dovuti al trascorrere degli anni, al precoce invecchiamento biologico, ed alla predisposizione genetica (1, 2, 11-25).
L’accelerazione dell’invecchiamento biologico, ad esempio, risulta maggiormente accentuata nelle persone che conducono stili di vita poco salutari, es.: alimentazione pro-infiammatoria, fumo, alcol, sedentarietà ecc. (26, 27).
L’invecchiamento precoce è a sua volta sostenuto dalla presenza di malattie, es.: cardiache, renali, diabete, post-ictus, depressione, disturbi del sonno ecc. (28-30), ma anche dall’eccesso di grasso corporeo (31), un’ulteriore causa di infiammazione cronica sistemica (32).
Anche i disturbi infiammatori della pelle possono propagarsi a livello sistemico, innescare alterazioni immunitarie, ridurre la produzione cutanea di importanti fattori necessari al mantenimento delle attività cerebrali (33-36).
Questi fenomeni possono essere aggravati dall’esposizione dell’organismo a fattori esterni all’organismo: microplastiche (37), abitudine al fumo e consumo di alcol (38, 39, 40), inquinanti ambientali (41-44), metalli pesanti, pesticidi (45), causa di danni diretti ai mitocondri ed altre strutture cellulari, inclusi i neuroni (45-52).
Inoltre, le sollecitazioni esterne, aumentano l’ossido-infiammazione, ed indeboliscono le difese antiossidanti del nostro organismo (59-63). Si tratta di un declino causato anche da un insufficiente introito di antiossidanti di origine alimentare che, come noto, è associato anche ad una ridotta cognitività (64, 65).
Viceversa l’adeguato consumo di antiossidanti dimostra effetti protettivi, come emerge da un’indagine svolta su circa 20.000 soggetti della National Health and Nutrition Examination Survey (NHANES) e confermata da altre ricerche pubblicate nel 2025 (64, 65).
Pertanto, risulta prioritario l’apporto di vitamine del gruppo B, vitamina C, E e D, coenzima Q10, omega 3, polifenoli ecc., in gran parte dotate di effetti antiossido-infiammatori, utili per l’omeostasi dei mitocondri e per la neuroprotezione (64-70).
Come noto vari fattori possono esporre al rischio di un’insufficiente assunzione di questi micronutrienti, di un aumentato fabbisogno, di un ridotto assorbimento (71, 72).
Molti altri fattori possono incidere sull’integrità dei mitocondri, ed aumentare il rischio di una ridotta performance cognitiva.
Ne sono un esempio gli alti livelli ematici di omocisteina (73-85) (Nota 1), contrastabili con un adeguato apporto alimentare e /o nutraceutico di vitamine B6, B12, e di folati / acido folico (86-93).
Queste vitamine dimostrano benefici anche contro la demenza vascolare (94-97).
L’acido folico, ad esempio, riducesignificativamente il rischio di malattie cerebrovascolari e dell’ictus, attraverso la normalizzazione del profilo lipidico, oltre a svolgere attività antiossidanti / antinfiammatorie (98).
Il coenzima Q10 e resveratrolo attenuano i processi patogenetici dell’aterosclerosi, attraverso la riattivazione dei mitocondri (99, 100).
Queste molecole combatto ulteriori meccanismi deleteri per la vita cellulare (101-110), dove risulta benefica anche la N-acetilcisteina (NAC) attraverso l’incremento dei livelli cellulari di glutatione (111-115).
I mitocondri risentono inoltre di particolari condizioni metaboliche ed ormonali, come nel caso della menopausa (116-123).
Per questo, già nel periodo riproduttivo, l’adeguato apporto di antiossidanti presenti negli alimenti e/o nutraceutici, e lo stile di vita, si confermano un intervento significativo per prevenire rallentare i fenomeni, che con il declino degli estrogeni tendono ad aggravarsi (124).
Il legame tra performance mitocondriale e cognitiva viene influenzato anche dall’equilibrio del microbiota intestinale (125-131), orale (129), e cutaneo (130).
Anche la letteratura 2026 conferma i benefici dei polifenoli, come il resveratrolo, sulla regolazione del microbiota intestinale (132-136).
La stabilizzazione della barriera e del microbiota intestinale è inoltre positivamente influenzata da adeguati livelli di vitamine (es.: B), polifenoli (es.: quercitina, resveratrolo), acidi grassi omega 3, probiotici, che vantano specifici contributi neuroprotettivi, contro la neuroinfiammazione e la performance cognitiva (137).
L’antiaging mitocondriale di Mitochon srl
I trattamenti centrati sui mitocondri sono da alcuni anni la modalità antiaging studiata dalla ricerca Mitochon srl https://www.mitochon.it/, ed utilizzata con successo per i propri cosmeceutici e nutraceutici contenenti coenzima Q10, resveratrolo, acido folico, vitamina C, N-acetilcisteina ecc. (1-10, 138-144).
L’integrazione selettiva delle vitamine e molecole bioattive dell’integratore orosolubile Mitofast® bit.ly/3VUlGkS,e quello liquido Mitofast B12 bit.ly/4d5ll4P, permette di compensare il frequente rischio di insufficiente apporto, il declino delle difese antiossidanti, oltre ad attenuare l’accelerazione dell’invecchiamento biologico e migliorare il benessere generale dell’organismo (71, 72, 140-150).
Nota 1(73, 90)
Fattori legati allo stile di vita come il consumo eccessivo di caffè ed alcol, l’abitudine al fumo e la mancanza di attività fisica possono influenzare il metabolismo dell'omocisteina, ed i suoi livelli plasmatici.
Di conseguenza, uno squilibrio nei livelli di omocisteina può portare all'iperomocisteinemia, una condizione caratterizzata da livelli elevati di omocisteina nel plasma, con valori normali da 5 a 15 µmol/L. I livelli elevati di omocisteinemia sono classificati come lievi (da 15 a 30 µmol/L), moderati (da 30 a 100 µmol/L) e gravi (superiori a 100 µmol/L).
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68. Shtilbans A. Combination Supplement Therapy: A New Frontier in Treatment of Neurodegenerative Diseases. J Nutr. 2025 Jul 15:S0022-3166(25)00427-4. doi: 10.1016/j.tjnut.2025.07.004.
69. Nankivell MC, Rosenfeldt F, Pipingas A, Pase MP, Reddan JM, Stough C. Coenzyme Q10 and Cognition: A Review. Nutrients. 2025 Sep 8;17(17):2896. doi: 10.3390/nu17172896.
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71. Mini-Review Motivi per l’Integrazione Mirata 2024 https://www.mitochon.it/4-motivi-1-per-utilizzare-lintegrazione-mirata-contro-linvecchiamento-cutaneo-e-sistemico/
72. Mini-Review studio pilota Mitofast 2024 https://www.mitochon.it/mitofast-nuovi-ed-importanti-risultati-da-uno-studio-clinico-preliminare/
73. Agostini D, Bartolacci A, Rotondo R, De Pandis MF, Battistelli M, Micucci M, Potenza L, Polidori E, Ferrini F, Sisti D, et al. Homocysteine, Nutrition, and Gut Microbiota: A Comprehensive Review of Current Evidence and Insights. Nutrients. 2025; 17(8):1325. https://doi.org/10.3390/nu17081325
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79. Li H, Chen Y, Wang Z, Wang Y, Bi R, Hou J, Chen H, Zhang Z, Guo Z, Chen Z, Cui H, Li S. Accelerated epigenetic aging as a modifier of homocysteine-associated cognitive decline: Findings from NHANES. Alzheimers Dement. 2026 Apr;22(4):e71349. doi: 10.1002/alz.71349.
80. Saija C, Currò M, Ientile R, Caccamo D, Bertuccio MP. Impact of Alterations in Homocysteine, Asymmetric Dimethylarginine and Vitamins-Related Pathways in Some Neurodegenerative Diseases: A Narrative Review. International Journal of Molecular Sciences. 2025; 26(8):3672. https://doi.org/10.3390/ijms26083672
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83. Decaix T, Lilamand M, Götze K, Mouton-Liger F, Cognat E, Hugon J, Bouaziz-Amar E, Sindzingre L, Dumurgier J, Paquet C. Unraveling Homocysteine's Role in Dementia: No Specific Association with Alzheimer's Disease, but a Connection to White Matter Hyperintensities. Aging Dis. 2025 Mar 5;17(2):1084-1093. doi: 10.14336/AD.225.0020.
84. Ramires Júnior OV, Prauchner GRK, Rieder AS, Leite AKO, Farias CP, Wyse ATS. Uncovering Hyperhomocysteinemia: Global Risk Patterns and Molecular Disruption in Brain and Vascular Health. J Neurochem. 2025 Dec;169(12):e70327. doi: 10.1111/jnc.70327.
85. Higgins Tejera C, Zhu P, Ware EB, Hicken MT, Zawistowski M, Kobayashi LC, Seblova D, Manly J, Mukherjee B, Bakulski KM. DNA methylation age acceleration mediates the relationship between systemic inflammation and cognitive impairment. Epigenomics. 2025 Dec;17(18):1399-1409. doi: 10.1080/17501911.2025.2595905.
86. Kacerova T, Yates AG, Dai J, Shepherd D, Pires E, de Jel S, Gong Q, Schiffer E, Jernerén F, Olsen T, De Jager Loots CA, Refsum H, Smith AD, McCullagh JSO, Anthony DC, Probert F. Role of B vitamins in modulating homocysteine and metabolic pathways linked to brain atrophy: Metabolomics insights from the VITACOG trial. Alzheimers Dement. 2025 Jul;21(7):e70521. doi: 10.1002/alz.70521.
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88. Zainuddin MS, Ghanesh K, Ganesan N, Kumari M, Radhakrishnan AK, Bhuvanendran S. Epigenetic modulations and nutrient interactions in Alzheimer's disease: unveiling potential therapeutic pathways. Nutr Neurosci. 2025 Dec;28(12): 1488-1510. doi: 10.1080/1028415X.2025.2526155.89. Khate K, Chaudhary V, Bhattacharjee D, Kaushik A, Walia GK, Babu N, Saraswathy KN, Devi NK. Global DNA Methylation and Cognitive Impairment: A Population-Based Study from Haryana, North India. Indian J Clin Biochem. 2025 Oct;40(4):651-659. doi: 10.1007/s12291-024-01205-z.
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94. Ihuoma J, Milan M, Negri S, Troyano-Rodriguez E, Rudraboina R, Kosmider A, Awasthi S, Csiszar A, Ungvari Z, Yabluchanskiy A, Balasubramanian P, Tarantini S. LDL oxidation and cerebrovascular aging: mechanisms of endothelial dysfunction, inflammation, and vascular cognitive impairment and dementia. Redox Biol. 2026 Mar 10;92:104118. doi: 10.1016/j.redox.2026.104118.
95. Gong Z, Chen Z, Sang S, Yang L, Qin H, Li Q, Jia Y. Mitochondrial DNA 6 mA methylation by METTL4 drives neuroinflammation via cGAS-STING activation in vascular cognitive impairment. Free Radic Biol Med. 2026 Mar 16;246:1-16. doi: 10.1016/j.freeradbiomed.2026.01.019.
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97. Chauhan R, Lidoo K, Jyoti U, Singh TG, Devi S. Decoding the gut microbiota-mitochondrial-inflammasome axis in cardiovascular disease. Mol Cell Biochem. 2026 Mar;481(3):1081-1101. doi: 10.1007/s11010-025-05451-4.
98. Federica Fogacci, Carmine Pizzi, Luca Bergamaschi, Valentina Di Micoli, Arrigo F.G. Cicero, Folic acid and plasma lipids: Interactions and effect of folate supplementation, Current Problems in Cardiology, Volume 49, Issue 6, 2024, https://doi.org/10.1016/j.cpcardiol.2024.102539.
99. Glogowski PA, Fogacci F, Algieri C, Cugliari A, Trombetti F, Nesci S, Cicero AFG. Reprogramming the Mitochondrion in Atherosclerosis: Targets for Vascular Protection. Antioxidants. 2025; 14(12):1462. https://doi.org/10.3390/antiox14121462
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101. Cui Y, Zhu P, Jiang M. Ferroptosis in Vascular Diseases: A Mechanistic and Immunological Perspective on Therapeutic Targeting. Antioxidants. 2026; 15(4):502. https://doi.org/10.3390/antiox15040502
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103. Fei Y, Leng Q. Research Progress of Ferroptosis in Cerebral Infarction. Brain Behav. 2026 Jan;16(1):e71192. doi: 10.1002/brb3.71192.
104. Zhou J, Shi W, Jiang Y, Yue R. Mechanisms and therapeutic strategies of ferroptosis in Diabetic-Associated Cognitive Dysfunction: focus on the crosstalk with apoptosis, autophagy, and pyroptosis. Mol Biol Rep. 2026 Jan 13;53(1):281. doi: 10.1007/s11033-026-11446-1.
105. Fang Y, Han Z, Yang S, Chen J, Li R, Zhang Z, Song J, Wang D, Ban Y. Ferroptosis and Alzheimer's disease: unraveling the molecular mechanisms and therapeutic opportunities. Front Cell Dev Biol. 2026 Jan 23;14:1758041. doi: 10.3389/fcell.2026.1758041.
106. Chen J, Shi Z, Chen Y, Xiong K, Wang Y, Zhang H. A CoQ10 analog ameliorates cognitive impairment and early brain injury after subarachnoid hemorrhage by regulating ferroptosis and neuroinflammation. Redox Biol. 2025 Jul;84:103684. doi: 10.1016/j.redox.2025.103684.
107. Mantle D. Coenzyme Q10 and Intracellular Signalling Pathways: Clinical Relevance. Int J Mol Sci. 2025 Nov 14;26(22):11024. doi: 10.3390/ijms262211024.
108. Zhou Z, Zhang Y, Liu S, Tang H, Yang L, Lu Y, Liao J, Zhang S, Chen Z, Yang L. Ferroptosis in Alzheimer's disease: molecular mechanisms and advances in therapeutic strategies. Front Neurosci. 2026 Jan 12;19:1673315. doi: 10.3389/fnins.2025.1673315.
109. Saadh MJ, Nazar Saeed T, Fawzi Al-Hussainy A, Kyada A, Ballal S, Kundlas M, Sabarivani A, Rizaev J, Ghalib Taher S, Alwan M, Jawad M, Mushtaq H. Mechanistic insights into ubiquinone Q10 in Parkinson's disease: mitochondrial protection, ferroptosis inhibition, and antioxidant recycling. Arch Physiol Biochem. 2026 Feb;132(1):134-150. doi: 10.1080/13813455.2025.2541698.
110. Wang Y, Zhang J, Wang Z, Ren Q, Li Z, Huang G, Li W. Folic Acid Ameliorates Neuronal Ferroptosis in Aging by Up-Regulating SLC7A11-GSH-GPX4 Antioxidant Pathway and Increasing Cystine Levels. Int J Mol Sci. 2025 Jul 11;26(14):6669. doi: 10.3390/ijms26146669.
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112. Zheng J, Zhang W, Ito J, Henkelmann B, Xu C, Mishima E, Conrad M. N-acetyl-l-cysteine averts ferroptosis by fostering glutathione peroxidase 4. Cell Chem Biol. 2025 May 15;32(5):767-775.e5. doi: 10.1016/j.chembiol.2025.04.002.
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118. Helio José Coelho-Junior, Emanuele Marzetti, Casey L. Sexton, Kevin Wu, Robert Mankowski, Stephen D. Anton, Christiaan Leeuwenburgh, Anna Picca, Mitochondrial quality control measures, systemic inflammation, and lower-limb muscle power in older adults: a PROMPT secondary analysis, The Journal of nutrition, health and aging, Volume 28, Issue 12, 2024, https://doi.org/10.1016/j.jnha.2024.100408.
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121. Yu Y, Yapeng H, Liu Z, Fang L, Li J, Luan Y, Li W, Cong H, Wu X. Mitochondrial dysfunction in perimenopausal mood disorders: From hormonal shifts to neuroenergetic failure (Review). Int J Mol Med. 2025 Dec;56(6):215. doi: 10.3892/ijmm.2025.5656.
122. Hao J, Liu L, Chang B, Zhao Y, Lai Y, Tian C, Xu H, Wang H, Ji L, Yang J. Blood-detected mitochondrial biomarker NSUN4: a potential indicator of ovarian aging. Exp Gerontol. 2025 Sep;208:112825. doi: 10.1016/j.exger.2025.112825.
123. Muhammad YA (2025) Reproductive aging in biological females: mechanisms and immediate consequences. Front. Endocrinol. 16:1658592. doi: 10.3389/fendo.2025.1658592
124. Rahman MA, Jalouli M, Al-Zharani M, Harrath AH. Next-Generation Dietary Antioxidants in Women’s Reproductive Health: Mechanisms, Reproductive Outcomes, and Therapeutic Potential. Antioxidants. 2026; 15(3):319. https://doi.org/10.3390/antiox15030319
125. Gupta P, Dutta S, Dutta K, Bhattacharjee P, Hazra A, Jash R. Interconnection between gut microbial metabolites and mitochondrial ROS production: implications for cellular health. Mol Cell Biochem. 2026 Jan;481(1):41-65. doi: 10.1007/s11010-025-05397-7.
126. Mir PA, Kumar N, Bhutia GT, Chaudhary P, Kaur G, Gupta SK. The aging gut-glia-immune axis in alzheimer's disease: microbiome-derived mediators of neuroinflammation and therapeutic innovation. Geroscience. 2026 Apr;48(2):2201-2241. doi: 10.1007/s11357-025-02062-1.
127. Czaj PV, Szewczyk-Golec K, Nuszkiewicz J, Woźniak A. Gut Dysbiosis and Microbiota-Derived Metabolites in Neurodegenerative Diseases: Molecular and Biochemical Mechanisms Along the Gut-Brain Axis. Molecules. 2026 Jan 30;31(3):490. doi: 10.3390/molecules31030490.
128. Mini-Review Vitamine complesso B - resveratrolo - microbiota 2024 https://www.mitochon.it/le-vitamine-del-gruppo-b-cosa-ce-di-nuovo-parte-2/
129. Mini-Review Salute orale - Invecchiamento 2025 https://www.mitochon.it/la-salute-orale-contro-linvecchiamento-e-le-malattie-correlate/?v=0d149b90e739
130. Mini-Review Pelle - Infiammazione cronica 2025 https://www.mitochon.it/la-pelle-come-scudo-contro-linfiammazione-cronica-dellorganismo/?v=0d149b90e739
131. Mini-Review Over 50 salute cutanea e benessere psicofisico 2025https://www.mitochon.it/la-salute-cutanea-negli-over-50-per-il-benessere-psicofisico/?v=0d149b90e739
132. Kogut Ł, Puchalski C, Katryńska D, Zaguła G. The Multidirectional Biological Activity of Resveratrol: Molecular Mechanisms, Systemic Effects and Therapeutic Potential-A Review. Nutrients. 2026 Jan 19;18(2):313. doi: 10.3390/nu18020313.
133. Tang P, Feng H, Zhang D, Wu J, Zhou Y, Feng W, Peng C. Dietary Polyphenols in Metabolic Diseases: Roles of Gut Microbiota-Derived Metabolites. Phytother Res. 2026 Mar;40(3):1408-1445. doi: 10.1002/ptr.70180.
134. Rudrapal M, de Oliveira AM, Singh RP. Dietary polyphenols maintain human health through modulation of gut microbiota. Front Pharmacol. 2026 Jan 5;16:1710088. doi: 10.3389/fphar.2025.1710088.
135. Toderescu CD, Parveen M, Trifunschi S, Oancea A, Jurj GCC, Cresneac IG, Munteanu MF, Ciopanoiu I, Boru C, Pogurschi EN, Ionite C, Stefanache A, Lungu II. Dietary Polyphenols as Modulators of Bifidobacterium in the Human Gut Microbiota. Nutrients. 2026 Feb 27;18(5):782. doi: 10.3390/nu18050782.
136. Wang Z, Ba S, Li M, Wei Y, Wang Y, Mao J, Xiang Y, Qin D, Zeng C. Targeting the Gut Microbiota: Mechanistic Investigation of Polyphenol Modulation of the Gut-Brain Axis in Alzheimer's Disease. Int J Mol Sci. 2026 Jan 7;27(2):604. doi: 10.3390/ijms27020604
137. Castillo-Moral Á, Toda-Ferran C, Bulló M, Teichenné J, Escoté X. Nutraceuticals and the Microbiota-Gut-Brain Axis: A Pathway for Preventing Cognitive Decline. Nutr Rev. 2026 Mar 24:nuag017. doi: 10.1093/nutrit/nuag017.
138. Kwaśniewska K, Fic W, Polak-Szczybyło E. Vitamins as Modulators of Neurodegenerative Disease Pathways: Mechanisms and Therapeutic Perspectives. Nutrients. 2026; 18(6):995. https://doi.org/10.3390/nu18060995
139. Zhou M, Zheng M, Liang S, Li M, Ma J, Zhang S, Song X, Hu Y, Lyu Y, Ou X, Yue C (2026) Inherent potential of mitochondria-targeted interventions for chronic neurodegenerative diseases. Neural Regen Res 21(4):1409-1427.
140. Mini-Review Resveratrolo - Età biologica / Coenzima Q10 disfunzione mitocondriale 2025 https://www.mitochon.it/resveratrolo-coenzima-q10-eta-biologica-mitocondri-cosa-ce-di-nuovo/?v=0d149b90e739
141. Hsu C-N, Tain Y-L. Resveratrol and Redox Regulation in Cardiovascular Disease Across the Life Course: Mechanistic and Translational Perspectives. Antioxidants. 2026; 15(4):509. https://doi.org/10.3390/antiox15040509
142. Li S, Hamaya R, Zhu H, Chen BH, Pereira AC, Ivey KL, Rist PM, Manson JE, Dong Y, Sesso HD. Effects of daily multivitamin-multimineral and cocoa extract supplementation on epigenetic aging clocks in the COSMOS randomized clinical trial. Nat Med. 2026 Mar;32(3):1012-1022. doi: 10.1038/s41591-026-04239-3
143. Miao J, Zhao D. Relationship Between Serum Vitamins and Cognitive Impairment in the Elderly: A Study Based on the NHANES Database. Brain Behav. 2026 Jan;16(1):e71181. doi: 10.1002/brb3.71181.
144. Ayoub G. Vitamins, Vascular Health and Disease. Nutrients. 2025 Sep 15;17(18):2955. doi: 10.3390/nu17182955.
145. Mini-Review Antiaging cognitivo 2025 https://www.mitochon.it/antiaging-cognitivo/?v=0d149b90e739
146. Mini-Review Antiaging cardiovascolare 2025 https://www.mitochon.it/antiaging-cardiovascolare/?v=0d149b90e739
147. Mini-Review Antiaging muscolare 2025 https://www.mitochon.it/antiaging-muscolare/?v=0d149b90e739
148. Mini-Review Osteoporosi - Resveratrolo 2025 https://www.mitochon.it/osteoporosi-nel-post-menopausa-attualita-sul-ruolo-del-resveratrolo-altri-antiossidanti-e-vitamine/?v=0d149b90e739
149. Mini-Review Sovrappenso / Obesità - Resveratrolo - Antiossidanti 2025 https://www.mitochon.it/sovrappeso-obesita-quale-contributo-dal-resveratrolo-ed-altri-antiossidanti/?v=0d149b90e739
150. Mini-Review Stress psicofisico - Antiossidanti / Neuroprotettori 2025 https://www.mitochon.it/stress-psicofisico-attualita-sulluso-appropriato-di-antiossidanti-neuroprotettivi/?v=0d149b90e739
autore Andrea Tognelli, Farmacista - Firenze****