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Page 22 of 29 Novati et al. Ageing Neur Dis 2022;2:17 https://dx.doi.org/10.20517/and.2022.19

onset parkinsonism. Ann Neurol 2004;56:427-31. DOI PubMed
90. Kondapalli C, Kazlauskaite A, Zhang N, et al. PINK1 is activated by mitochondrial membrane potential depolarization and stimulates
Parkin E3 ligase activity by phosphorylating Serine 65. Open Biol 2012;2:120080. DOI PubMed PMC
91. Gautier CA, Kitada T, Shen J. Loss of PINK1 causes mitochondrial functional defects and increased sensitivity to oxidative stress.
Proc Natl Acad Sci U S A 2008;105:11364-9. DOI PubMed PMC
92. Amo T, Sato S, Saiki S, et al. Mitochondrial membrane potential decrease caused by loss of PINK1 is not due to proton leak, but to
respiratory chain defects. Neurobiol Dis 2011;41:111-8. DOI PubMed
93. Kane LA, Lazarou M, Fogel AI, et al. PINK1 phosphorylates ubiquitin to activate Parkin E3 ubiquitin ligase activity. J Cell Biol
2014;205:143-53. DOI PubMed PMC
94. Wang XL, Feng ST, Wang ZZ, Yuan YH, Chen NH, Zhang Y. Parkin, an E3 ubiquitin ligase, plays an essential role in mitochondrial
quality control in Parkinson’s disease. Cell Mol Neurobiol 2021;41:1395-411. DOI PubMed
95. Heo JY, Park JH, Kim SJ, et al. DJ-1 null dopaminergic neuronal cells exhibit defects in mitochondrial function and structure:
involvement of mitochondrial complex I assembly. PLoS One 2012;7:e32629. DOI PubMed PMC
96. Hayashi T, Ishimori C, Takahashi-Niki K, et al. DJ-1 binds to mitochondrial complex I and maintains its activity. Biochem Biophys
Res Commun 2009;390:667-72. DOI PubMed
97. Poulopoulos M, Levy OA, Alcalay RN. The neuropathology of genetic Parkinson’s disease. Mov Disord 2012;27:831-42. DOI
PubMed PMC
98. Villeneuve LM, Purnell PR, Boska MD, Fox HS. Early expression of Parkinson’s disease-related mitochondrial abnormalities in
PINK1 knockout rats. Mol Neurobiol 2016;53:171-86. DOI PubMed PMC
99. Gispert S, Ricciardi F, Kurz A, et al. Parkinson phenotype in aged PINK1-deficient mice is accompanied by progressive
mitochondrial dysfunction in absence of neurodegeneration. PLoS One 2009;4:e5777. DOI PubMed PMC
100. Kitada T, Tong Y, Gautier CA, Shen J. Absence of nigral degeneration in aged parkin/DJ-1/PINK1 triple knockout mice. J
Neurochem 2009;111:696-702. DOI PubMed PMC
101. Dave KD, De Silva S, Sheth NP, et al. Phenotypic characterization of recessive gene knockout rat models of Parkinson’s disease.
Neurobiol Dis 2014;70:190-203. DOI PubMed
102. Almikhlafi MA, Stauch KL, Villeneuve LM, Purnell PR, Lamberty BG, Fox HS. Deletion of DJ-1 in rats affects protein abundance
and mitochondrial function at the synapse. Sci Rep 2020;10:13719. DOI PubMed PMC
103. Chandran JS, Lin X, Zapata A, et al. Progressive behavioral deficits in DJ-1-deficient mice are associated with normal nigrostriatal
function. Neurobiol Dis 2008;29:505-14. DOI PubMed PMC
104. Kim RH, Smith PD, Aleyasin H, et al. Hypersensitivity of DJ-1-deficient mice to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyrindine
(MPTP) and oxidative stress. Proc Natl Acad Sci U S A 2005;102:5215-20. DOI PubMed PMC
105. Chen L, Cagniard B, Mathews T, et al. Age-dependent motor deficits and dopaminergic dysfunction in DJ-1 null mice. J Biol Chem
2005;280:21418-26. DOI PubMed
106. Goldberg MS, Fleming SM, Palacino JJ, et al. Parkin-deficient mice exhibit nigrostriatal deficits but not loss of dopaminergic
neurons. J Biol Chem 2003;278:43628-35. DOI
107. Yu-Taeger L, Petrasch-Parwez E, Osmand AP, et al. A novel BACHD transgenic rat exhibits characteristic neuropathological
features of Huntington disease. J Neurosci 2012;32:15426-38. DOI PubMed PMC
108. von Horsten S, Schmitt I, Nguyen HP, Holzmann C, Schmidt T, et al. Transgenic rat model of Huntington’s disease. Hum Mol Genet
2003;12:617-24. DOI PubMed
109. Teo RT, Hong X, Yu-Taeger L, et al. Structural and molecular myelination deficits occur prior to neuronal loss in the YAC128 and
BACHD models of Huntington disease. Hum Mol Genet 2016;25:2621-32. DOI PubMed PMC
110. Blockx I, Van Camp N, Verhoye M, et al. Genotype specific age related changes in a transgenic rat model of Huntington’s disease.
Neuroimage 2011;58:1006-16. DOI PubMed
111. Clemens LE, Weber JJ, Wlodkowski TT, et al. Olesoxime suppresses calpain activation and mutant huntingtin fragmentation in the
BACHD rat. Brain 2015;138:3632-53. DOI PubMed
112. Petrasch-Parwez E, Nguyen HP, Löbbecke-Schumacher M, et al. Cellular and subcellular localization of Huntingtin [corrected]
aggregates in the brain of a rat transgenic for Huntington disease. J Comp Neurol 2007;501:716-30. DOI
113. Ruiz-Opazo N, Kosik KS, Lopez LV, Bagamasbad P, Ponce LR, Herrera VL. Attenuated hippocampus-dependent learning and
memory decline in transgenic TgAPPswe Fischer-344 rats. Mol Med 2004;10:36-44. DOI PubMed PMC
114. Wang CE, Tydlacka S, Orr AL, et al. Accumulation of N-terminal mutant huntingtin in mouse and monkey models implicated as a
pathogenic mechanism in Huntington’s disease. Hum Mol Genet 2008;17:2738-51. DOI PubMed PMC
115. Kuiper EF, de Mattos EP, Jardim LB, Kampinga HH, Bergink S. Chaperones in polyglutamine aggregation: beyond the Q-stretch.
Front Neurosci 2017;11:145. DOI PubMed PMC
116. Bondi MW, Jak AJ, Delano-Wood L, Jacobson MW, Delis DC, Salmon DP. Neuropsychological contributions to the early
identification of Alzheimer’s disease. Neuropsychol Rev 2008;18:73-90. DOI PubMed PMC
117. Skelton WP 3rd, Skelton NK. Alzheimer’s disease. Recognizing and treating a frustrating condition. Postgrad Med 1991;90:33-4, 37.
DOI PubMed
118. Lithfous S, Dufour A, Després O. Spatial navigation in normal aging and the prodromal stage of Alzheimer’s disease: insights from
imaging and behavioral studies. Ageing Res Rev 2013;12:201-13. DOI PubMed