REFERENCES
1. Daviglus ML, Bell CC, Berrettini W, et al. National Institutes of Health State-of-the-Science Conference statement: preventing alzheimer disease and cognitive decline. Ann Intern Med 2010;153:176-81.
2. Arvanitakis Z. The need to better understand aging and risk factors for dementia. Front Dement 2024;2:1346281.
3. Clouston SAP, Richmond LL, Scott SB, et al. Pattern recognition to objectively differentiate the etiology of cognitive decline: analysis of the impact of stroke and Alzheimer’s disease. Neuroepidemiology 2020;54:446-53.
5. Ferrucci L, Fabbri E. Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty. Nat Rev Cardiol 2018;15:505-22.
6. Webster GC, Webster SL. Decreased protein synthesis by microsomes from aging Drosophila melanogaster. Exp Gerontol 1979;14:343-8.
7. Ekstrom R, Liu DS, Richardson A. Changes in brain protein synthesis during the life span of male Fischer rats. Gerontology 1980;26:121-8.
8. Mukaetova-Ladinska EB, Harrington CR, Roth M, Wischik CM. Alterations in tau protein metabolism during normal aging. Dementia 1996;7:95-103.
9. Chiu MJ, Fan LY, Chen TF, Chen YF, Chieh JJ, Horng HE. Plasma tau levels in cognitively normal middle-aged and older adults. Front Aging Neurosci 2017;9:51.
10. Mink JW, Blumenschine RJ, Adams DB. Ratio of central nervous system to body metabolism in vertebrates: its constancy and functional basis. Am J Physiol 1981;241:R203-12.
12. Harman D. Aging: a theory based on free radical and radiation chemistry. Sci Aging Knowl Environ 2002;2002:cp14.
13. Anik MI, Mahmud N, Masud AA, et al. Role of reactive oxygen species in aging and age-related diseases: a review. ACS Appl Bio Mater 2022;5:4028-54.
14. Wei Y, Miao Q, Zhang Q, et al. Aerobic glycolysis is the predominant means of glucose metabolism in neuronal somata, which protects against oxidative damage. Nat Neurosci 2023;26:2081-9.
15. Vaishnavi SN, Vlassenko AG, Rundle MM, Snyder AZ, Mintun MA, Raichle ME. Regional aerobic glycolysis in the human brain. Proc Natl Acad Sci U S A 2010;107:17757-62.
16. Descalzi G, Gao V, Steinman MQ, Suzuki A, Alberini CM. Lactate from astrocytes fuels learning-induced mRNA translation in excitatory and inhibitory neurons. Commun Biol 2019;2:247.
17. Brown AM, Ransom BR. Astrocyte glycogen as an emergency fuel under conditions of glucose deprivation or intense neural activity. Metab Brain Dis 2015;30:233-9.
18. Heiden MG, Cantley LC, Thompson CB. Understanding the Warburg effect: the metabolic requirements of cell proliferation. Science 2009;324:1029-33.
19. Shannon BJ, Vaishnavi SN, Vlassenko AG, Shimony JS, Rutlin J, Raichle ME. Brain aerobic glycolysis and motor adaptation learning. Proc Natl Acad Sci U S A 2016;113:e3782-91.
20. Li D, Ding Z, Gui M, Hou Y, Xie K. Metabolic enhancement of glycolysis and mitochondrial respiration are essential for neuronal differentiation. Cell Reprogram 2020;22:291-9.
21. Goyal MS, Hawrylycz M, Miller JA, Snyder AZ, Raichle ME. Aerobic glycolysis in the human brain is associated with development and neotenous gene expression. Cell Metab 2014;19:49-57.
22. Pellerin L, Magistretti PJ. Glutamate uptake into astrocytes stimulates aerobic glycolysis: a mechanism coupling neuronal activity to glucose utilization. Proc Natl Acad Sci U S A 1994;91:10625-9.
23. Horvat A, Muhič M, Smolič T, et al. Ca2+ as the prime trigger of aerobic glycolysis in astrocytes. Cell Calcium 2021;95:102368.
24. Ma W, Berg J, Yellen G. Ketogenic diet metabolites reduce firing in central neurons by opening K(ATP) channels. J Neurosci 2007;27:3618-25.
25. Ramezani M, Fernando M, Eslick S, et al. Ketone bodies mediate alterations in brain energy metabolism and biomarkers of Alzheimer’s disease. Front Neurosci 2023;17:1297984.
26. Ma S, Suzuki K. Keto-adaptation and endurance exercise capacity, fatigue recovery, and exercise-induced muscle and organ damage prevention: a narrative review. Sports 2019;7:40.
27. Klosinski LP, Yao J, Yin F, et al. White matter lipids as a ketogenic fuel supply in aging female brain: implications for Alzheimer’s disease. EBioMedicine 2015;2:1888-904.
28. Vodičková A, Koren SA, Wojtovich AP. Site-specific mitochondrial dysfunction in neurodegeneration. Mitochondrion 2022;64:1-18.
31. Weingarten MD, Lockwood AH, Hwo SY, Kirschner MW. A protein factor essential for microtubule assembly. Proc Natl Acad Sci U S A 1975;72:1858-62.
32. Tracy TE, Madero-Pérez J, Swaney DL, et al. Tau interactome maps synaptic and mitochondrial processes associated with neurodegeneration. Cell 2022;185:712-28.e14.
33. Mosconi L, De Santi S, Li J, et al. Hippocampal hypometabolism predicts cognitive decline from normal aging. Neurobiol Aging 2008;29:676-92.
34. Hammond TC, Xing X, Wang C, et al. β-amyloid and tau drive early Alzheimer’s disease decline while glucose hypometabolism drives late decline. Commun Biol 2020;3:352.
35. Minoshima S, Giordani B, Berent S, Frey KA, Foster NL, Kuhl DE. Metabolic reduction in the posterior cingulate cortex in very early Alzheimer’s disease. Ann Neurol 1997;42:85-94.
36. Rocher AB, Chapon F, Blaizot X, Baron JC, Chavoix C. Resting-state brain glucose utilization as measured by PET is directly related to regional synaptophysin levels: a study in baboons. Neuroimage 2003;20:1894-8.
37. Farfel JM, Yu L, De Jager PL, Schneider JA, Bennett DA. Association of APOE with tau-tangle pathology with and without β-amyloid. Neurobiol Aging 2016;37:19-25.
38. Shi Y, Yamada K, Liddelow SA, et al; Alzheimer’s Disease Neuroimaging Initiative. ApoE4 markedly exacerbates tau-mediated neurodegeneration in a mouse model of tauopathy. Nature 2017;549:523-7.
39. Goyal MS, Vlassenko AG, Blazey TM, et al. Loss of brain aerobic glycolysis in normal human aging. Cell Metab 2017;26:353-60.e3.
41. Dukart J, Mueller K, Villringer A, et al; Alzheimer’s Disease Neuroimaging Initiative. Relationship between imaging biomarkers, age, progression and symptom severity in Alzheimer’s disease. Neuroimage Clin 2013;3:84-94.
42. Beyer L, Meyer-Wilmes J, Schönecker S, et al. Clinical routine FDG-PET imaging of suspected progressive supranuclear palsy and corticobasal degeneration: a gatekeeper for subsequent tau-PET imaging? Front Neurol 2018;9:483.
43. Braak H, Braak E. Neuropathological stageing of Alzheimer-related changes. Acta Neuropathol 1991;82:239-59.
44. Tahmasian M, Pasquini L, Scherr M, et al. The lower hippocampus global connectivity, the higher its local metabolism in Alzheimer disease. Neurology 2015;84:1956-63.
45. Apostolova I, Lange C, Mäurer A, et al; Alzheimer’s Disease Neuroimaging Initiative. Hypermetabolism in the hippocampal formation of cognitively impaired patients indicates detrimental maladaptation. Neurobiol Aging 2018;65:41-50.
46. Choi EJ, Son YD, Noh Y, Lee H, Kim YB, Park KH. Glucose hypometabolism in hippocampal subdivisions in Alzheimer’s disease: a pilot study using high-resolution 18F-FDG PET and 7.0-T MRI. J Clin Neurol 2018;14:158-64.
47. Chen Y, Wang J, Cui C, et al. Evaluating the association between brain atrophy, hypometabolism, and cognitive decline in Alzheimer’s disease: a PET/MRI study. Aging 2021;13:7228-46.
48. Baghel V, Tripathi M, Parida G, et al. In vivo assessment of tau deposition in Alzheimer disease and assessing its relationship to regional brain glucose metabolism and cognition. Clin Nucl Med 2019;44:e597-601.
49. Ackley SF, Zimmerman SC, Brenowitz WD, et al. Effect of reductions in amyloid levels on cognitive change in randomized trials: instrumental variable meta-analysis. BMJ 2021;372:n156.
50. Lauretti E, Praticò D. Glucose deprivation increases tau phosphorylation via P38 mitogen-activated protein kinase. Aging Cell 2015;14:1067-74.
51. Maphis N, Jiang S, Xu G, et al. Selective suppression of the α isoform of p38 MAPK rescues late-stage tau pathology. Alzheimers Res Ther 2016;8:54.
52. Son SH, Lee NR, Gee MS, et al. Chemical knockdown of phosphorylated p38 mitogen-activated protein kinase (MAPK) as a novel approach for the treatment of Alzheimer’s disease. ACS Cent Sci 2023;9:417-26.
53. Coulthard LR, White DE, Jones DL, McDermott MF, Burchill SA. p38(MAPK): stress responses from molecular mechanisms to therapeutics. Trends Mol Med 2009;15:369-79.
54. ClinicalTrials.gov. Search results. Showing results for: T3D-959. Available from: https://clinicaltrials.gov/search?intr=T3D-959. [Last accessed on 30 Apr 2024].
55. Yan Z, Ni Y, Wang P, et al. Peroxisome proliferator-activated receptor delta protects against obesity-related glomerulopathy through the P38 MAPK pathway. Obesity 2013;21:538-45.
56. Fan M, Rhee J, St-Pierre J, et al. Suppression of mitochondrial respiration through recruitment of p160 myb binding protein to PGC-1alpha: modulation by p38 MAPK. Genes Dev 2004;18:278-89.
57. Combs B, Mueller RL, Morfini G, Brady ST, Kanaan NM. Tau and axonal transport misregulation in tauopathies. Adv Exp Med Biol 2019;1184:81-95.
58. Sabui A, Biswas M, Somvanshi PR, et al. Decreased anterograde transport coupled with sustained retrograde transport contributes to reduced axonal mitochondrial density in tauopathy neurons. Front Mol Neurosci 2022;15:927195.
59. DuBoff B, Götz J, Feany MB. Tau promotes neurodegeneration via DRP1 mislocalization in vivo. Neuron 2012;75:618-32.
60. Li XC, Hu Y, Wang ZH, et al. Human wild-type full-length tau accumulation disrupts mitochondrial dynamics and the functions via increasing mitofusins. Sci Rep 2016;6:24756.
61. Cummins N, Tweedie A, Zuryn S, Bertran-Gonzalez J, Götz J. Disease-associated tau impairs mitophagy by inhibiting Parkin translocation to mitochondria. EMBO J 2019;38:e99360.
62. Rhein V, Song X, Wiesner A, et al. Amyloid-beta and tau synergistically impair the oxidative phosphorylation system in triple transgenic Alzheimer’s disease mice. Proc Natl Acad Sci U S A 2009;106:20057-62.
63. Esteras N, Rohrer JD, Hardy J, Wray S, Abramov AY. Mitochondrial hyperpolarization in iPSC-derived neurons from patients of FTDP-17 with 10+16 MAPT mutation leads to oxidative stress and neurodegeneration. Redox Biol 2017;12:410-22.
64. Demetrius LA, Simon DK. An inverse-Warburg effect and the origin of Alzheimer’s disease. Biogerontology 2012;13:583-94.
65. Harris RA, Tindale L, Cumming RC. Age-dependent metabolic dysregulation in cancer and Alzheimer’s disease. Biogerontology 2014;15:559-77.
66. Zhang X, Wu L, Swerdlow RH, Zhao L. Opposing effects of ApoE2 and ApoE4 on glycolytic metabolism in neuronal aging supports a warburg neuroprotective cascade against Alzheimer’s disease. Cells 2023;12:410.
67. Fisher-Wellman KH, Neufer PD. Linking mitochondrial bioenergetics to insulin resistance via redox biology. Trends Endocrinol Metab 2012;23:142-53.
68. Bonen A, Parolin ML, Steinberg GR, et al. Triacylglycerol accumulation in human obesity and type 2 diabetes is associated with increased rates of skeletal muscle fatty acid transport and increased sarcolemmal FAT/CD36. FASEB J 2004;18:1144-6.
69. Van der Jeugd A, Parra-Damas A, Baeta-Corral R, et al. Reversal of memory and neuropsychiatric symptoms and reduced tau pathology by selenium in 3xTg-AD mice. Sci Rep 2018;8:6431.
70. Wu, Zhe Ying, Gomez-Pinilla F. Vitamin E protects against oxidative damage and learning disability after mild traumatic brain injury in rats. Neurorehabil Neural Repair 2010;24:290-8.
71. Melov S, Adlard PA, Morten K, et al. Mitochondrial oxidative stress causes hyperphosphorylation of tau. PLoS One 2007;2:e536.
72. Chandrasekaran K, Hatanpää K, Brady DR, Rapoport SI. Evidence for physiological down-regulation of brain oxidative phosphorylation in Alzheimer’s disease. Exp Neurol 1996;142:80-8.
73. Manczak M, Park BS, Jung Y, Reddy PH. Differential expression of oxidative phosphorylation genes in patients with Alzheimer’s disease: implications for early mitochondrial dysfunction and oxidative damage. Neuromolecular Med 2004;5:147-62.
74. Mahapatra G, Gao Z, Bateman JR 3rd, et al. Blood-based bioenergetic profiling reveals differences in mitochondrial function associated with cognitive performance and Alzheimer’s disease. Alzheimers Dement 2023;19:1466-78.
75. Lee H, Cho S, Kim MJ, et al. ApoE4-dependent lysosomal cholesterol accumulation impairs mitochondrial homeostasis and oxidative phosphorylation in human astrocytes. Cell Rep 2023;42:113183.
76. Yang J, Ruchti E, Petit JM, et al. Lactate promotes plasticity gene expression by potentiating NMDA signaling in neurons. Proc Natl Acad Sci U S A 2014;111:12228-33.
77. Harris RA, Tindale L, Lone A, et al. Aerobic glycolysis in the frontal cortex correlates with memory performance in wild-type mice but not the APP/PS1 mouse model of cerebral amyloidosis. J Neurosci 2016;36:1871-8.
78. Zheng J, Xie Y, Ren L, et al. GLP-1 improves the supportive ability of astrocytes to neurons by promoting aerobic glycolysis in Alzheimer’s disease. Mol Metab 2021;47:101180.
79. Vlassenko AG, Gordon BA, Goyal MS, et al. Aerobic glycolysis and tau deposition in preclinical Alzheimer’s disease. Neurobiol Aging 2018;67:95-8.
80. Siraj MA, Mundil D, Beca S, et al. Cardioprotective GLP-1 metabolite prevents ischemic cardiac injury by inhibiting mitochondrial trifunctional protein-α. J Clin Invest 2020;130:1392-404.
81. Farmer BC, Williams HC, Devanney NA, et al. APOΕ4 lowers energy expenditure in females and impairs glucose oxidation by increasing flux through aerobic glycolysis. Mol Neurodegener 2021;16:62.
82. Cho S, Lee H, Seo J. Impact of genetic risk factors for Alzheimer’s disease on brain glucose metabolism. Mol Neurobiol 2021;58:2608-19.
83. Ercoli L, Siddarth P, Huang SC, et al. Perceived loss of memory ability and cerebral metabolic decline in persons with the apolipoprotein E-IV genetic risk for Alzheimer disease. Arch Gen Psychiatry 2006;63:442-8.
84. Grimm A. Impairments in brain bioenergetics in aging and Tau pathology: a chicken and egg situation? Cells 2021;10:2531.
85. Dougherty RJ, Schultz SA, Kirby TK, et al. Moderate physical activity is associated with cerebral glucose metabolism in adults at risk for Alzheimer’s disease. J Alzheimers Dis 2017;58:1089-97.
86. Feng S, Wu C, Zou P, et al. High-intensity interval training ameliorates Alzheimer’s disease-like pathology by regulating astrocyte phenotype-associated AQP4 polarization. Theranostics 2023;13:3434-50.
87. Gibala MJ, McGee SL, Garnham AP, Howlett KF, Snow RJ, Hargreaves M. Brief intense interval exercise activates AMPK and p38 MAPK signaling and increases the expression of PGC-1alpha in human skeletal muscle. J Appl Physiol 2009;106:929-34.
88. Gurd BJ, Menezes ES, Arhen BB, Islam H. Impacts of altered exercise volume, intensity, and duration on the activation of AMPK and CaMKII and increases in PGC-1α mRNA. Semin Cell Dev Biol 2023;143:17-27.
89. Frederiksen KS, Gjerum L, Waldemar G, Hasselbalch SG. Physical activity as a moderator of Alzheimer pathology: a systematic review of observational studies. Curr Alzheimer Res 2019;16:362-78.
90. Liu Y, Chu JMT, Yan T, et al. Short-term resistance exercise inhibits neuroinflammation and attenuates neuropathological changes in 3xTg Alzheimer’s disease mice. J Neuroinflammation 2020;17:4.
91. Wu C, Yang L, Tucker D, et al. Beneficial effects of exercise pretreatment in a sporadic Alzheimer’s rat model. Med Sci Sports Exerc 2018;50:945-56.
92. Jeong JH, Koo JH, Cho JY, Kang EB. Neuroprotective effect of treadmill exercise against blunted brain insulin signaling, NADPH oxidase, and Tau hyperphosphorylation in rats fed a high-fat diet. Brain Res Bull 2018;142:374-83.
93. Brown BM, Rainey-Smith SR, Dore V, et al. Self-reported physical activity is associated with Tau burden measured by positron emission tomography. J Alzheimers Dis 2018;63:1299-305.
94. Brown BM, Peiffer J, Rainey-Smith SR. Exploring the relationship between physical activity, beta-amyloid and tau: a narrative review. Ageing Res Rev 2019;50:9-18.
95. Pietrzak D, Kasperek K, Rękawek P, Piątkowska-Chmiel I. The therapeutic role of ketogenic diet in neurological disorders. Nutrients 2022;14:1952.
96. Lin AL, Zhang W, Gao X, Watts L. Caloric restriction increases ketone bodies metabolism and preserves blood flow in aging brain. Neurobiol Aging 2015;36:2296-303.
97. Krikorian R, Shidler MD, Dangelo K, Couch SC, Benoit SC, Clegg DJ. Dietary ketosis enhances memory in mild cognitive impairment. Neurobiol Aging 2012;33:425.e19-27.
98. Reger MA, Henderson ST, Hale C, et al. Effects of beta-hydroxybutyrate on cognition in memory-impaired adults. Neurobiol Aging 2004;25:311-4.
99. Henderson ST, Vogel JL, Barr LJ, Garvin F, Jones JJ, Costantini LC. Study of the ketogenic agent AC-1202 in mild to moderate Alzheimer’s disease: a randomized, double-blind, placebo-controlled, multicenter trial. Nutr Metab 2009;6:31.
100. Kashiwaya Y, Bergman C, Lee JH, et al. A ketone ester diet exhibits anxiolytic and cognition-sparing properties, and lessens amyloid and tau pathologies in a mouse model of Alzheimer’s disease. Neurobiol Aging 2013;34:1530-9.
101. Pawlosky RJ, Kashiwaya Y, King MT, Veech RL. A dietary ketone ester normalizes abnormal behavior in a mouse model of Alzheimer’s disease. Int J Mol Sci 2020;21:1044.
102. Limongi F, Siviero P, Bozanic A, Noale M, Veronese N, Maggi S. The effect of adherence to the mediterranean diet on late-life cognitive disorders: a systematic review. J Am Med Dir Assoc 2020;21:1402-9.
103. Shannon OM, Ranson JM, Gregory S, et al. Mediterranean diet adherence is associated with lower dementia risk, independent of genetic predisposition: findings from the UK Biobank prospective cohort study. BMC Med 2023;21:81.
104. Kang J, Jia T, Jiao Z, et al. Increased brain volume from higher cereal and lower coffee intake: shared genetic determinants and impacts on cognition and metabolism. Cereb Cortex 2022;32:5163-74.
105. Agarwal P, Leurgans SE, Agrawal S, et al. Association of mediterranean-DASH intervention for neurodegenerative delay and mediterranean diets with Alzheimer disease pathology. Neurology 2023;100:e2259-68.
106. Tauffenberger A, Fiumelli H, Almustafa S, Magistretti PJ. Lactate and pyruvate promote oxidative stress resistance through hormetic ROS signaling. Cell Death Dis 2019;10:653.
107. Huang Z, Zhang Y, Zhou R, Yang L, Pan H. Lactate as potential mediators for exercise-induced positive effects on neuroplasticity and cerebrovascular plasticity. Front Physiol 2021;12:656455.
108. Bonomi CG, De Lucia V, Mascolo AP, et al. Brain energy metabolism and neurodegeneration: hints from CSF lactate levels in dementias. Neurobiol Aging 2021;105:333-9.
109. Malm J, Kristensen B, Ekstedt J, Adolfsson R, Wester P. CSF monoamine metabolites, cholinesterases and lactate in the adult hydrocephalus syndrome (normal pressure hydrocephalus) related to CSF hydrodynamic parameters. J Neurol Neurosurg Psychiatry 1991;54:252-9.
110. Parnetti L, Gaiti A, Polidori MC, et al. Increased cerebrospinal fluid pyruvate levels in Alzheimer’s disease. Neurosci Lett 1995;199:231-3.
111. Redjems-Bennani N, Jeandel C, Lefebvre E, Blain H, Vidailhet M, Guéant JL. Abnormal substrate levels that depend upon mitochondrial function in cerebrospinal fluid from Alzheimer patients. Gerontology 1998;44:300-4.
112. Liguori C, Stefani A, Sancesario G, Sancesario GM, Marciani MG, Pierantozzi M. CSF lactate levels, τ proteins, cognitive decline: a dynamic relationship in Alzheimer’s disease. J Neurol Neurosurg Psychiatry 2015;86:655-9.
113. Zebhauser PT, Berthele A, Goldhardt O, et al. Cerebrospinal fluid lactate levels along the Alzheimer’s disease continuum and associations with blood-brain barrier integrity, age, cognition, and biomarkers. Alzheimers Res Ther 2022;14:61.
114. Helbok R, Schiefecker A, Delazer M, et al. Cerebral tau is elevated after aneurysmal subarachnoid haemorrhage and associated with brain metabolic distress and poor functional and cognitive long-term outcome. J Neurol Neurosurg Psychiatry 2015;86:79-86.
115. Xu D, Vincent A, González-Gutiérrez A, et al. A monocarboxylate transporter rescues frontotemporal dementia and Alzheimer’s disease models. PLoS Genet 2023;19:e1010893.
116. de Geus MB, Leslie SN, Lam T, et al. Mass spectrometry in cerebrospinal fluid uncovers association of glycolysis biomarkers with Alzheimer’s disease in a large clinical sample. Sci Rep 2023;13:22406.
117. Bergau N, Maul S, Rujescu D, Simm A, Navarrete Santos A. Reduction of glycolysis intermediate concentrations in the cerebrospinal fluid of Alzheimer’s disease patients. Front Neurosci 2019;13:871.
118. Nielsen JE, Andreassen T, Gotfredsen CH, et al. Serum metabolic signatures for Alzheimer’s disease reveal alterations in amino acid composition: a validation study. Metabolomics 2024;20:12.
119. Wang X, Hu X, Yang Y, Takata T, Sakurai T. Systemic pyruvate administration markedly reduces neuronal death and cognitive impairment in a rat model of Alzheimer’s disease. Exp Neurol 2015;271:145-54.
120. Koivisto H, Leinonen H, Puurula M, et al. Corrigendum: Chronic pyruvate supplementation increases exploratory activity and brain energy reserves in young and middle-aged mice. Front Aging Neurosci 2017;9:67.
121. Isopi E, Granzotto A, Corona C, et al. Pyruvate prevents the development of age-dependent cognitive deficits in a mouse model of Alzheimer’s disease without reducing amyloid and tau pathology. Neurobiol Dis 2015;81:214-24.
122. Edwards ES, Sackett SC. Psychosocial variables related to why women are less active than men and related health implications. Clin Med Insights Womens Health 2016;9:47-56.
123. Edwards HM, Wallace CE, Gardiner WD, et al. Sex-dependent effects of acute stress on amyloid-β in male and female mice. Brain 2023;146:2268-74.
124. Sharma K, Akre S, Chakole S, Wanjari MB. Stress-induced diabetes: a review. Cureus 2022;14:e29142.
125. Chen X, Jiang H. Tau as a potential therapeutic target for ischemic stroke. Aging 2019;11:12827-43.
126. Randall J, Mörtberg E, Provuncher GK, et al. Tau proteins in serum predict neurological outcome after hypoxic brain injury from cardiac arrest: results of a pilot study. Resuscitation 2013;84:351-6.
127. Jiang Y, Zhu Z, Shi J, et al. Metabolomics in the development and progression of dementia: a systematic review. Front Neurosci 2019;13:343.
128. Zhang X, Hu W, Wang Y, et al. Plasma metabolomic profiles of dementia: a prospective study of 110,655 participants in the UK Biobank. BMC Med 2022;20:252.
