Page 27 - AN-1-3
P. 27

Advanced Neurology                                           Early inhibition of PDK1 prevents AD-like pathology



            13.  Yao YL, Wang YX, Yang FC, et al., 2022, Targeting AKT   27.  Lawlor MA, Mora A, Ashby PR, et al., 2002, Essential role
               and CK2 represents a novel therapeutic strategy for SMO   of PDK1 in regulating cell size and development in mice.
               constitutive activation-driven medulloblastoma.  CNS   EMBO J, 21: 3728–3738.
               Neurosci Ther, 28: 1033–1044.                   28.  Xu C, Yu L, Hou J, et al., 2017, Conditional deletion of PDK1
            14.  Wang J, Yu Z, Tao Y, et al., 2021, A novel palmitic acid   in the forebrain causes neuron loss and increased apoptosis
               hydroxy stearic acid (5-PAHSA) plays a neuroprotective   during cortical development. Front Cell Neurosci, 11: 330.
               role by inhibiting phosphorylation of the m-TOR-ULK1   29.  Wei YJ, Han XN, Zhao CJ, 2020, PDK1 regulates the survival
               pathway and regulating autophagy.  CNS Neurosci Ther,   of the developing cortical interneurons. Mol Brain, 13: 65.
               27: 484–496.
                                                               30.  Oakley H, Cole SL, Logan S, et al., 2006, Intraneuronal-
            15.  Wang H, Liu M, Zou G, et al., 2021, Deletion of PDK1   amyloid aggregates, neurodegeneration, and neuron loss
               in oligodendrocyte lineage cells causes white matter   in transgenic mice with five familial Alzheimer’s disease
               abnormality and myelination defect in the central nervous   mutations: Potential factors in amyloid plaque formation.
               system. Neurobiol Dis, 148: 105212.                J Neurosci, 26: 10129–10140.
            16.  Wang H, Liu M, Ye Z, et al., 2021, Akt regulates Sox10   31.  Liu T, Zhu X, Huang C, et al., 2022, ERK inhibition reduces
               expression to control oligodendrocyte differentiation via   neuronal death and ameliorates inflammatory responses in
               phosphorylating FoxO1. J Neurosci, 41: 8163–8180.  forebrain-specific Ppp2cα knockout mice. FASEB J, e222515.
            17.  Ma Y, Xu X, Li C, et al., 2021, Induced neural progenitor cell-  32.  Huang C, Liu T, Wang Q, et al., 2020, Loss of PP2A disrupts
               derived extracellular vesicles promote neural progenitor cell   the retention of radial glial progenitors in the telencephalic
               survival  via  extracellular  signal-regulated  kinase  pathway.   niche to impair the generation for late-born neurons during
               CNS Neurosci Ther, 27: 1605–1609.                  cortical development. Cereb Cortex, 30: 4183–4196.
            18.  Fedder-Semmes KN, Appel B, 2021, The Akt-mTOR   33.  Cheng S, Liu T, Hu, Y, et al., 2019, Conditional inactivation
               pathway drives myelin sheath growth by regulating Cap-  of Pen-2 in the developing neocortex leads to rapid switch of
               dependent translation. J Neurosci, 41: 8532.       apical progenitors to basal progenitors. J Neurosci, 39: 2195–
            19.  Bonet  IJ,  Khomula  EV,  Araldi  D, et al.,  2021,  PI3K/AKT   2207.
               signaling in high molecular weight hyaluronan (HMWH)-  34.  Englund C, Fink A, Lau C, et al., 2005, Pax6, Tbr2, and
               induced anti-hyperalgesia and reversal of nociceptor   Tbr1 are expressed sequentially by radial glia, intermediate
               sensitization. J Neurosci, 41: 8414.               progenitor  cells,  and postmitotic  neurons  in developing
            20.  Zhao XF, Liao Y, Alam MM, et al., 2020, Microglial mTOR is   neocortex. J Neurosci, 25: 247–251.
               neuronal protective and antiepileptogenic in the pilocarpine   35.  Wu J, Shao C, Ye X, et al., 2021, In vivo brain imaging of
               model of temporal lobe epilepsy. J Neurosci, 40: 7593.  amyloid-aggregates  in Alzheimer’s  disease  with  a near-
            21.  Fruman DA, Chiu H, Hopkins BD, et al., 2017, The PI3K   infrared fluorescent probe. ACS Sensors, 6: 863–870.
               pathway in human disease. Cell, 170: 605–635.   36.  Ma X, Wang Y, Hua J, et al., 2020, Abeta-sheet-targeted
            22.  Pietri M, Dakowski C, Hannaoui S, et al., 2013, PDK1   theranostic agent for diagnosing and preventing aggregation
               decreases TACE-mediated alpha-secretase activity and   of pathogenic peptides in Alzheimer’s disease. Sci CHINA
               promotes disease progression in prion and Alzheimer’s   Chem, 63: 73–82.
               diseases. Nat Med, 19: 1124–1131.               37.  Ye X, Chen L, Wang H, et al., 2022, Genetic inhibition of
            23.  Pei JJ, Khatoon S, An WL, et al., 2003, Role of protein   PDK1 robustly reduces plaque deposition and ameliorates
               kinase B in Alzheimer’s neurofibrillary pathology.  Acta   gliosis in the 5×FAD mouse model of Alzheimer’s disease.
               Neuropathol, 105: 381–392.                         Neuropathol Appl Neurobiol, 48: e12839.
            24.  Mathys H, Davila-Velderrain J, Peng Z, et al., 2019, Single-  38.  Han X, Wei Y, Ba R, et al., 2021, PDK1 regulates the
               cell transcriptomic analysis of Alzheimer’s disease. Nature,   lengthening of G1 phase to balance RGC proliferation and
               570: 332–337.                                      differentiation during cortical neurogenesis. Cereb Cortex,
                                                                  32: 3488–3500.
            25.  Yang S, Pascual-Guiral S, Ponce R, et al., 2018, Reducing the
               levels of Akt activation by PDK1 knock-in mutation protects   39.  Han X, Wei Y, Wu X, et al., 2020, PDK1 regulates transition
               neuronal cultures against synthetic smyloid-beta peptides.   period of apical progenitors to basal progenitors by controlling
               Front Aging Neurosci, 9, 435.                      asymmetric cell division. Cereb Cortex, 30: 406–420.
            26.  Stein TD, Johnson, JA, 2002, Lack of neurodegeneration in   40.  Wang L, Cheng S, Yin Z, et al., 2015, Conditional inactivation
               transgenic mice overexpressing mutant amyloid precursor   of Akt three isoforms causes tau hyperphosphorylation in
               protein is associated with increased levels of transthyretin   the brain. Mol Neurodegener, 10: 33.
               and  the activation  of cell survival pathways.  J  Neurosci,   41.  Li QQ, Chen J, Hu P, et al., 2022, Enhancing GluN2A-
               22: 7380.                                          type NMDA receptors impairs long-term synaptic plasticity and


            Volume 1 Issue 3 (2022)                         11                      https://doi.org/10.36922/an.v1i3.153
   22   23   24   25   26   27   28   29   30   31   32