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AD is characterized by the progressive decline of memory and multiple cognitive functions, and changes in behavior and personality. Recent research has revealed age\u2010dependent increased levels of VDAC1 in postmortem AD brains and cerebral cortices of APP, APPxPS1, and 3xAD.Tg mice. Further, we found abnormal interaction between VDAC1 and P\u2010Tau in the AD brains, leading to mitochondrial structural and functional defects. Our current study aimed to understand the impact of a partial reduction of voltage\u2010dependent anion channel 1 (VDAC1) protein on mitophagy\/autophagy, mitochondrial and synaptic activities, and behavior changes in transgenic TAU mice in Alzheimer's disease. To determine if a partial reduction of VDAC1 reduces mitochondrial and synaptic toxicities in transgenic Tau (P301L) mice, we crossed heterozygote VDAC1 knockout (VDAC1<jats:sup>+\/\u2212<\/jats:sup>) mice with TAU mice and generated double mutant (VDAC1<jats:sup>+\/\u2212<\/jats:sup>\/TAU) mice. We assessed phenotypic behavior, protein levels of mitophagy, autophagy, synaptic, other key proteins, mitochondrial morphology, and dendritic spines in TAU mice relative to double mutant mice. Partial reduction of VDAC1 rescued the TAU\u2010induced behavioral impairments such as motor coordination and exploratory behavioral changes, and learning and spatial memory impairments in VDAC1<jats:sup>+\/\u2212<\/jats:sup>\/TAU mice. Protein levels of mitophagy, autophagy, and synaptic proteins were significantly increased in double mutant mice compared with TAU mice. In addition, dendritic spines were significantly increased; the mitochondrial number was significantly reduced, and mitochondrial length was increased in double mutant mice. Based on these observations, we conclude that reduced VDAC1 is beneficial in symptomatic\u2010transgenic TAU mice.<\/jats:p>","DOI":"10.1111\/acel.13663","type":"journal-article","created":{"date-parts":[[2022,7,8]],"date-time":"2022-07-08T06:45:58Z","timestamp":1657262758000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":39,"title":["A partial reduction of <scp>VDAC1<\/scp> enhances mitophagy, autophagy, synaptic activities in a transgenic Tau mouse model"],"prefix":"10.1111","volume":"21","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7426-3415","authenticated-orcid":false,"given":"Murali","family":"Vijayan","sequence":"first","affiliation":[{"name":"Department of Internal Medicine Texas Tech University Health Sciences Center  Lubbock Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rainier Vladlen","family":"Alvir","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Texas Tech University Health Sciences Center  Lubbock Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Razelle Veronique","family":"Alvir","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Texas Tech University Health Sciences Center  Lubbock Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lloyd E.","family":"Bunquin","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Texas Tech University Health Sciences Center  Lubbock Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jangampalli Adi","family":"Pradeepkiran","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Texas Tech University Health Sciences Center  Lubbock Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9560-9948","authenticated-orcid":false,"given":"P. 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