Login Register Cart 0
Generic placeholder image

Current Pharmaceutical Design

Editor-in-Chief

ISSN (Print): 1381-6128
ISSN (Online): 1873-4286

Back
Journal Home About Journal Editorial Board Journal Insight Current Issue Volumes/Issues
Subscribe
Review Article

The Relationship between SNAP25 and Some Common Human Neurological Syndromes

Author(s): Jie Shu, Fan Peng, Jing Li, Yuhang Liu, Xiaolan Li* and Chengfu Yuan*

Volume 30, Issue 30, 2024

Published on: 03 July, 2024

Page: [2378 - 2386] Pages: 9

DOI: 10.2174/0113816128305683240621060024

Price: $65

Abstract

Over the years, research on the pathogenesis of neurological diseases has progressed slowly worldwide. However, as the incidence rate continues to increase and the disease gradually develops, early diagnosis and treatment have become a top priority. SANP25, a protein present on the presynaptic membrane and involved in neurotransmitter release, is closely related to the loss or abnormal expression of synapses and neurons. SNAP25 deficiency can lead to synaptic disorders and inhibit neurotransmitter release. Therefore, a large amount of literature believes that SNAP25 gene mutation is a risk factor for many neurological diseases. This review used advanced search on PubMed to conduct extensive article searches for relevant literature. The search keywords included SNAP25 and Alzheimer's disease, SNAP25 and Parkinson's disease, and so on. After reading and summarizing the previous papers, the corresponding conclusions were obtained to achieve the purpose of the review. The deficiency or variation of SNAP25 might be related to the onset of schizophrenia, epilepsy, attention deficit/hypoactivity disorder, bipolar disorder effective disorder, and autism. SNAP25 has been found to be used as a neuropathological marker for neurological diseases, which could be the target of diagnosis or treatment of Alzheimer’s disease and Parkinson’s disease. Cerebrospinal Fluid (CSF) or blood has been found to enable more effective drug development.

« Previous Next »
[1]
Alten B, Zhou Q, Shin OH, et al. Role of aberrant spontaneous neurotransmission in SNAP25-associated encephalopathies. Neuron 2021; 109(1): 59-72.e5.
[http://dx.doi.org/10.1016/j.neuron.2020.10.012] [PMID: 33147442]
[2]
Houenou J, Boisgontier J, Henrion A, et al. A multilevel functional study of a SNAP25 at-risk variant for bipolar disorder and schizophrenia. J Neurosci 2017; 37(43): 10389-97.
[http://dx.doi.org/10.1523/JNEUROSCI.1040-17.2017] [PMID: 28972123]
[3]
Uzay B, Kavalali ET. Genetic disorders of neurotransmitter release machinery. Front Synaptic Neurosci 2023; 15: 1148957.
[http://dx.doi.org/10.3389/fnsyn.2023.1148957] [PMID: 37066095]
[4]
McGrowder DA, Miller F, Vaz K, et al. Cerebrospinal fluid biomarkers of Alzheimer’s disease: Current evidence and future perspectives. Brain Sci 2021; 11(2): 215.
[http://dx.doi.org/10.3390/brainsci11020215] [PMID: 33578866]
[5]
Kovács-Nagy R, Hu J, Rónai Z, Sasvári-Székely M. SNAP-25: A novel candidate gene in psychiatric genetics. Neuropsychopharmacol Hung 2009; 11(2): 89-94.
[PMID: 19827316]
[6]
Zhang H, Zhu S, Zhu Y, Chen J, Zhang G, Chang H. An association study between SNAP-25 gene and attention-deficit hyperactivity disorder. Eur J Paediatr Neurol 2011; 15(1): 48-52.
[http://dx.doi.org/10.1016/j.ejpn.2010.06.001] [PMID: 20599404]
[7]
Zhang H, Therriault J, Kang MS, et al. Cerebrospinal fluid synaptosomal-associated protein 25 is a key player in synaptic degeneration in mild cognitive impairment and Alzheimer’s disease. Alzheimers Res Ther 2018; 10(1): 80.
[http://dx.doi.org/10.1186/s13195-018-0407-6] [PMID: 30115118]
[8]
Antonucci F, Corradini I, Fossati G, Tomasoni R, Menna E, Matteoli M. SNAP-25, a known presynaptic protein with emerging postsynaptic functions. Front Synaptic Neurosci 2016; 8: 7.
[http://dx.doi.org/10.3389/fnsyn.2016.00007] [PMID: 27047369]
[9]
Høgh P. Alzheimer’s disease. Ugeskr Laeger 2017; 179(12): V09160686.
[PMID: 28330540]
[10]
Lane CA, Hardy J, Schott JM. Alzheimer’s disease. Eur J Neurol 2018; 25(1): 59-70.
[http://dx.doi.org/10.1111/ene.13439] [PMID: 28872215]
[11]
Apostolova LG, Hwang KS, Andrawis JP, et al. 3D PIB and CSF biomarker associations with hippocampal atrophy in ADNI subjects. Neurobiol Aging 2010; 31(8): 1284-303.
[http://dx.doi.org/10.1016/j.neurobiolaging.2010.05.003] [PMID: 20538372]
[12]
Ballard C, Gauthier S, Corbett A, Brayne C, Aarsland D, Jones E. Alzheimer’s disease. Lancet 2011; 377(9770): 1019-31.
[http://dx.doi.org/10.1016/S0140-6736(10)61349-9] [PMID: 21371747]
[13]
Wang Q, Tao S, Xing L, et al. SNAP25 is a potential target for early stage Alzheimer’s disease and Parkinson’s disease. Eur J Med Res 2023; 28(1): 570.
[http://dx.doi.org/10.1186/s40001-023-01360-8] [PMID: 38053192]
[14]
Sui X, Liu J, Yang X. Cerebrospinal fluid biomarkers of Alzheimer’s disease. Neurosci Bull 2014; 30(2): 233-42.
[http://dx.doi.org/10.1007/s12264-013-1412-1] [PMID: 24733653]
[15]
Najera K, Fagan BM, Thompson PM. SNAP-25 in major psychiatric disorders: A review. Neuroscience 2019; 420: 79-85.
[http://dx.doi.org/10.1016/j.neuroscience.2019.02.008] [PMID: 30790667]
[16]
Öhrfelt A, Brinkmalm A, Dumurgier J, et al. A novel ELISA for the measurement of cerebrospinal fluid SNAP-25 in patients with Alzheimer’s disease. Neuroscience 2019; 420: 136-44.
[http://dx.doi.org/10.1016/j.neuroscience.2018.11.038] [PMID: 30528858]
[17]
Blennow K, Zetterberg H. Biomarkers for Alzheimer’s disease: Current status and prospects for the future. J Intern Med 2018; 284(6): 643-63.
[http://dx.doi.org/10.1111/joim.12816] [PMID: 30051512]
[18]
Karmakar S, Sharma LG, Roy A, Patel A, Pandey LM. Neuronal SNARE complex: A protein folding system with intricate protein-protein interactions, and its common neuropathological hallmark, SNAP25. Neurochem Int 2019; 122: 196-207.
[http://dx.doi.org/10.1016/j.neuint.2018.12.001] [PMID: 30517887]
[19]
Pereira JB, Janelidze S, Ossenkoppele R, et al. Untangling the association of amyloid-β and tau with synaptic and axonal loss in Alzheimer’s disease. Brain 2021; 144(1): 310-24.
[http://dx.doi.org/10.1093/brain/awaa395] [PMID: 33279949]
[20]
Agostini S, Mancuso R, Liuzzo G, et al. Serum miRNAs expression and SNAP-25 genotype in Alzheimer’s disease. Front Aging Neurosci 2019; 11: 52.
[http://dx.doi.org/10.3389/fnagi.2019.00052] [PMID: 30914946]
[21]
Ren Z, Yu J, Wu Z, et al. MicroRNA-210-5p contributes to cognitive impairment in early vascular dementia rat model through targeting snap25. Front Mol Neurosci 2018; 11: 388.
[http://dx.doi.org/10.3389/fnmol.2018.00388] [PMID: 30483048]
[22]
Jia L, Zhu M, Kong C, et al. Blood neuro-exosomal synaptic proteins predict Alzheimer’s disease at the asymptomatic stage. Alzheimers Dement 2021; 17(1): 49-60.
[http://dx.doi.org/10.1002/alz.12166] [PMID: 32776690]
[23]
Fowler KD, Funt JM, Artyomov MN, Zeskind B, Kolitz SE, Towfic F. Leveraging existing data sets to generate new insights into Alzheimer’s disease biology in specific patient subsets. Sci Rep 2015; 5(1): 14324.
[http://dx.doi.org/10.1038/srep14324] [PMID: 26395074]
[24]
Brinkmalm A, Brinkmalm G, Honer WG, et al. SNAP-25 is a promising novel cerebrospinal fluid biomarker for synapse degeneration in Alzheimer’s disease. Mol Neurodegener 2014; 9(1): 53.
[http://dx.doi.org/10.1186/1750-1326-9-53] [PMID: 25418885]
[25]
Hayes MT. Parkinson’s disease and parkinsonism. Am J Med 2019; 132(7): 802-7.
[http://dx.doi.org/10.1016/j.amjmed.2019.03.001] [PMID: 30890425]
[26]
Beitz JM. Parkinson's disease a review. Front Biosci 2014; S6(1): 65-74.
[http://dx.doi.org/10.2741/S415] [PMID: 24389262]
[27]
Tolosa E, Garrido A, Scholz SW, Poewe W. Challenges in the diagnosis of Parkinson’s disease. Lancet Neurol 2021; 20(5): 385-97.
[http://dx.doi.org/10.1016/S1474-4422(21)00030-2] [PMID: 33894193]
[28]
Nakata Y, Yasuda T, Fukaya M, et al. Accumulation of α-synuclein triggered by presynaptic dysfunction. J Neurosci 2012; 32(48): 17186-96.
[http://dx.doi.org/10.1523/JNEUROSCI.2220-12.2012] [PMID: 23197711]
[29]
Garcia-Reitböck P, Anichtchik O, Bellucci A, et al. SNARE protein redistribution and synaptic failure in a transgenic mouse model of Parkinson’s disease. Brain 2010; 133(7): 2032-44.
[http://dx.doi.org/10.1093/brain/awq132] [PMID: 20534649]
[30]
Caminiti SP, Presotto L, Baroncini D, et al. Axonal damage and loss of connectivity in nigrostriatal and mesolimbic dopamine pathways in early Parkinson’s disease. Neuroimage Clin 2017; 14: 734-40.
[http://dx.doi.org/10.1016/j.nicl.2017.03.011] [PMID: 28409113]
[31]
Agliardi C, Meloni M, Guerini FR, et al. Oligomeric α-Syn and SNARE complex proteins in peripheral extracellular vesicles of neural origin are biomarkers for Parkinson’s disease. Neurobiol Dis 2021; 148: 105185.
[http://dx.doi.org/10.1016/j.nbd.2020.105185] [PMID: 33217562]
[32]
Gorenberg EL, Chandra SS. The role of co-chaperones in synaptic proteostasis and neurodegenerative disease. Front Neurosci 2017; 11: 248.
[http://dx.doi.org/10.3389/fnins.2017.00248] [PMID: 28579939]
[33]
Bereczki E, Bogstedt A, Höglund K, et al. Synaptic proteins in CSF relate to Parkinson’s disease stage markers. NPJ Parkinsons Dis 2017; 3(1): 7.
[http://dx.doi.org/10.1038/s41531-017-0008-2] [PMID: 28649607]
[34]
Huang J, Liu L, Qin L, Huang H, Li X. Weighted gene coexpression network analysis uncovers critical genes and pathways for multiple brain regions in Parkinson’s disease. BioMed Res Int 2021; 2021: 1-46.
[http://dx.doi.org/10.1155/2021/6616434] [PMID: 33791366]
[35]
Richetto J, Meyer U. Epigenetic modifications in schizophrenia and related disorders: Molecular scars of environmental exposures and source of phenotypic variability. Biol Psychiatry 2021; 89(3): 215-26.
[http://dx.doi.org/10.1016/j.biopsych.2020.03.008] [PMID: 32381277]
[36]
Owen MJ, Sawa A, Mortensen PB. Schizophrenia. Lancet 2016; 388(10039): 86-97.
[http://dx.doi.org/10.1016/S0140-6736(15)01121-6] [PMID: 26777917]
[37]
Yang H, Zhang M, Shi J, et al. Brain-specific SNAP-25 deletion leads to elevated extracellular glutamate level and schizophrenia like behavior in mice. Neural Plast 2017; 2017: 1-11.
[http://dx.doi.org/10.1155/2017/4526417] [PMID: 29318050]
[38]
Condliffe SB, Matteoli M. Inactivation kinetics of voltage-gated calcium channels in glutamatergic neurons are influenced by SNAP-25. Channels 2011; 5(4): 304-7.
[http://dx.doi.org/10.4161/chan.5.4.16228] [PMID: 21558797]
[39]
Ramos-Miguel A, Gicas K, Alamri J, et al. Reduced SNAP25 protein fragmentation contributes to SNARE complex dysregulation in schizophrenia postmortem brain. Neuroscience 2019; 420: 112-28.
[http://dx.doi.org/10.1016/j.neuroscience.2018.12.015] [PMID: 30579835]
[40]
Barakauskas VE, Moradian A, Barr AM, et al. Quantitative mass spectrometry reveals changes in SNAP-25 isoforms in schizophrenia. Schizophr Res 2016; 177(1-3): 44-51.
[http://dx.doi.org/10.1016/j.schres.2016.03.002] [PMID: 26971072]
[41]
Ramos-Miguel A, Barakauskas V, Alamri J, et al. The SNAP25 interactome in ventromedial caudate in schizophrenia includes the mitochondrial protein ARF1. Neuroscience 2019; 420: 97-111.
[http://dx.doi.org/10.1016/j.neuroscience.2018.12.045] [PMID: 30610939]
[42]
Xu C, Sellgren CM, Fatouros-Bergman H, et al. CSF levels of synaptosomal-associated protein 25 and synaptotagmin-1 in first-episode psychosis subjects. IBRO Rep 2020; 8: 136-42.
[http://dx.doi.org/10.1016/j.ibror.2020.04.001] [PMID: 32490278]
[43]
Barakauskas VE, Beasley CL, Barr AM, et al. A novel mechanism and treatment target for presynaptic abnormalities in specific striatal regions in schizophrenia. Neuropsychopharmacology 2010; 35(5): 1226-38.
[http://dx.doi.org/10.1038/npp.2009.228] [PMID: 20072114]
[44]
Hirschfeld RM, Vornik LA. Bipolar disorder-costs and comorbidity. Am J Manag Care 2005; 11(3) (Suppl.): S85-90.
[PMID: 16097719]
[45]
Barnett JH, Smoller JW. The genetics of bipolar disorder. Neuroscience 2009; 164(1): 331-43.
[http://dx.doi.org/10.1016/j.neuroscience.2009.03.080] [PMID: 19358880]
[46]
Etain B, Dumaine A, Mathieu F, et al. A SNAP25 promoter variant is associated with early-onset bipolar disorder and a high expression level in brain. Mol Psychiatry 2010; 15(7): 748-55.
[http://dx.doi.org/10.1038/mp.2008.148] [PMID: 19125158]
[47]
Bozzi Y, Casarosa S, Caleo M. Epilepsy as a neurodevelopmental disorder. Front Psychiatry 2012; 3: 19.
[http://dx.doi.org/10.3389/fpsyt.2012.00019] [PMID: 22457654]
[48]
Watanabe S, Yamamori S, Otsuka S, et al. Epileptogenesis and epileptic maturation in phosphorylation site-specific SNAP-25 mutant mice. Epilepsy Res 2015; 115: 30-44.
[http://dx.doi.org/10.1016/j.eplepsyres.2015.05.004] [PMID: 26220374]
[49]
Sabers A, Kjær TW. Epilepsy. Ugeskr Laeger 2014; 176(26): V11120634.
[PMID: 25294573]
[50]
Hamdan FF, Myers CT, Cossette P, et al. High rate of recurrent de novo mutations in developmental and epileptic encephalopathies. Am J Hum Genet 2017; 101(5): 664-85.
[http://dx.doi.org/10.1016/j.ajhg.2017.09.008] [PMID: 29100083]
[51]
Klöckner C, Sticht H, Zacher P, et al. De novo variants in SNAP25 cause an early-onset developmental and epileptic encephalopathy. Genet Med 2021; 23(4): 653-60.
[http://dx.doi.org/10.1038/s41436-020-01020-w] [PMID: 33299146]
[52]
Corradini I, Verderio C, Sala M, Wilson MC, Matteoli M. SNAP-25 in neuropsychiatric disorders. Ann N Y Acad Sci 2009; 1152(1): 93-9.
[http://dx.doi.org/10.1111/j.1749-6632.2008.03995.x] [PMID: 19161380]
[53]
Hawi Z, Matthews N, Wagner J, et al. DNA variation in the SNAP25 gene confers risk to ADHD and is associated with reduced expression in prefrontal cortex. PLoS One 2013; 8(4): e60274.
[http://dx.doi.org/10.1371/journal.pone.0060274] [PMID: 23593184]
[54]
Puentes-Rozo PJ, Acosta-López JE, Cervantes-Henríquez ML, et al. Genetic variation underpinning ADHD risk in a caribbean community. Cells 2019; 8(8): 907.
[http://dx.doi.org/10.3390/cells8080907] [PMID: 31426340]
[55]
Herken H, Erdal ME, Kenar ANİ, et al. Association of SNAP-25 gene Dde l and Mnl l polymorphisms with adult attention deficit hyperactivity disorder. Psychiatry Investig 2014; 11(4): 476-80.
[http://dx.doi.org/10.4306/pi.2014.11.4.476] [PMID: 25395980]
[56]
Forero DA, Arboleda GH, Vasquez R, Arboleda H. Candidate genes involved in neural plasticity and the risk for attention-deficit hyperactivity disorder: A meta-analysis of 8 common variants. J Psychiatry Neurosci 2009; 34(5): 361-6.
[PMID: 19721846]
[57]
Li J, Yan WJ, Wu Y, Tian XX, Zhang YW. Synaptosomal-associated protein 25 gene polymorphisms affect treatment efficiency of methylphenidate in children with attention-deficit hyperactivity disorder: An fNIRS study. Front Behav Neurosci 2022; 15: 793643.
[http://dx.doi.org/10.3389/fnbeh.2021.793643] [PMID: 35069142]
[58]
Thapar A, Rutter M. Genetic advances in autism. J Autism Dev Disord 2021; 51(12): 4321-32.
[http://dx.doi.org/10.1007/s10803-020-04685-z] [PMID: 32940822]
[59]
Bolognesi E, Guerini FR, Carta A, et al. The role of SNAP-25 in autism spectrum disorders onset patterns. Int J Mol Sci 2023; 24(18): 14042.
[http://dx.doi.org/10.3390/ijms241814042] [PMID: 37762342]
[60]
LeBlanc JJ, Fagiolini M. Autism: A “critical period” disorder? Neural Plast 2011; 2011: 1-17.
[http://dx.doi.org/10.1155/2011/921680] [PMID: 21826280]
[61]
Lenart J, Bratek E, Lazarewicz JW, Zieminska E. Changes in the expression of snap-25 protein in the brain of juvenile rats in two models of autism. J Mol Neurosci 2020; 70(9): 1313-20.
[http://dx.doi.org/10.1007/s12031-020-01543-6] [PMID: 32367505]
[62]
Braida D, Guerini FR, Ponzoni L, et al. Association between SNAP-25 gene polymorphisms and cognition in autism: Functional consequences and potential therapeutic strategies. Transl Psychiatry 2015; 5(1): e500.
[http://dx.doi.org/10.1038/tp.2014.136] [PMID: 25629685]
[63]
Choi MG, Kim MJ, Kim DG, Yu R, Jang YN, Oh WJ. Sequestration of synaptic proteins by alpha-synuclein aggregates leading to neurotoxicity is inhibited by small peptide. PLoS One 2018; 13(4): e0195339.
[http://dx.doi.org/10.1371/journal.pone.0195339] [PMID: 29608598]
[64]
Condliffe SB, Corradini I, Pozzi D, Verderio C, Matteoli M. Endogenous SNAP-25 regulates native voltage-gated calcium channels in glutamatergic neurons. J Biol Chem 2010; 285(32): 24968-76.
[http://dx.doi.org/10.1074/jbc.M110.145813] [PMID: 20522554]

Rights & Permissions Print Cite
© 2024 Bentham Science Publishers | Privacy Policy