Kelly Stauch, Ph.D.

Kelly Stauch, PhDKelly Stauch, Ph.D.
Assistant Professor and Seahorse Core Director

Durham Research Center, 3013
985800 Nebraska Medical Center
Omaha, NE  68198-5800


Keywords: Aging, Bioenergetics, Mitochondria, Neurodegeneration, Proteomics, Synapses

Research Interests
On-going projects
Visit Dr. Stauch's lab

Currently recruiting graduate students. Please contact if you are interested. 

Research Interests

My major focus is the role of mitochondrial dysfunction and altered energy metabolism in the context of neurodegenerative diseases and aging. Mitochondrial abnormalities are implicated to play a major role in aging and age-related neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease (PD). Further, HIV appears to increase the risk for several age-associated diseases, including cognitive impairment and antiretroviral drugs are associated with neurotoxic side effects, including mitochondrial toxicity, which likely contribute to the development of HIV-associated neurocognitive disorders (HAND). The goal of my work in the laboratory is to elucidate the mechanisms leading to alterations in mitochondrial energy metabolism in order to develop therapeutic strategies to treat or prevent neurodegeneration.

On-going projects

We are currently working on a project to investigate the mechanisms underlying age-associated presynaptic mitochondrial impairment in the context of tau pathology. The current pharmacological treatments for Alzheimer's Disease do not slow or stop the damage and destruction of neurons that cause symptoms and make the disease fatal. Despite evidence that pathologic tau accumulation and synaptic alterations correlate with cognitive deficits, the mechanisms underlying such alterations remain incompletely characterized; thus, our studies are designed to fill this gap in our knowledge.

We are also examining the impact of overexpression of Parkin, a multifaceted E3 ubiquitin ligase, on several parameters of mitochondrial health in the brain as a strategy to treat or prevent Parkinson's Disease (PD). Loss-of-function mutations in the gene encoding the Parkin protein lead to juvenile-onset autosomal recessive forms of PD and evidence suggests that Parkin functions as a protective agent by promoting mitochondrial health. We are further studying the effects of Pink1 and/or Parkin deficiency on parameters of mitochondrial health and function, specifically within nerve terminals. The Pink1/Parkin pathways appear key in PD pathogenesis as well as prevention/treatment paradigms.

Another project involves investigating the causal mechanisms underlying antiretroviral (ARV)-induced synaptic dysfunction, focusing on mitochondrial bioenergetics, metabolism, and neurotransmission, as a contributor to neurotoxicity. The number of ARV treated individuals living with HIV is increasing, thus understanding the contribution of ARV treatment to the development of the neurotoxicity observed in treated patients with HIV-associated neurocognitive disorders (HAND) has strong clinical implications.


Stauch KL, Emanuel K, Lamberty BG, Morsey B, and Fox HS. Central nervous system-penetrating antiretrovirals impair energetic reserve in striatal nerve terminals. J Neurovirol. 2017 Dec;23(6):795-807. PMID: 28895059

Stauch KL, Villeneuve LM, Purnell PR, Pandey S, Guda C, and Fox HS. SWATH-MS proteome profiling data comparison of DJ-1, Parkin, and PINK1 knockout rat striatal mitochondria. Data Brief. 2016 Sep 23; 9:589-593. PMID 27761515.

Stauch KL, Villeneuve LM, Purnell PR, Ottemann BM, Emanuel K, and Fox HS. Loss of Pink1 modulates synaptic mitochondrial bioenergetics in the rat striatum prior to motor symptoms: concomitant complex I respiratory defects and increased complex II-mediated respiration. Proteomics Clin Appl. 2016 Aug 28. Epub ahead of print. PMID: 27568932.

Li H, Spagnol G, Zheng L, Stauch KL, and Sorgen PL. Regulation of Connexin43 Function and Expression by Tyrosine Kinase 2. J Biol Chem. 2016 Jul 22; 291 (30): 15867-80. PMID: 27235399.

Ivanisevic J, Stauch KL, Petrascheck M, Benton HP, Epstein AA, Fang M, Gorantla S, Tran M, Hoang L, Kurczy ME, Boska MD, Gendelman HE, Fox HS, and Siuzdak G. Metabolic drift in the aging brain. Aging. 2016 May; 8 (5): 1000-20. PMID: 27182841.

Villeneuve LM, Purnell PR, Stauch KL, and Fox HS. Neonatal mitochondrial abnormalities due to Pink1 deficiency: Proteomics reveals early changes relevant to Parkinson’s disease. Data Brief. 2015 Dec 17; 6: 428-32. PMID: 26866053.

Villeneuve LM, Purnell PR, Stauch KL, Callen SE, Buch SJ, and Fox HS. HIV-1 transgenic rats display mitochondrial abnormalities consistent with abnormal energy generation and distribution. J Neurovirol. 2016 Oct; 22 (5): 564-574. PMID: 26843384.

Spagnol G, Kieken F, Kopanic JL, Li H, Zach S, Stauch KL, Grosely R, and Sorgen PL. Structural Studies of the Nedd4 WW Domains and Their Selectivity for the Connexin43 (Cx43) Carboxyl Terminus. J Biol Chem. 2016 Apr 1; 291 (14): 7637-50. PMID: 26841867.

Spagnol G, Al-Mugotir M, Kopanic JL, Zach S, Li H, Trease AJ, Stauch KL, Grosely R, Cervantes M, and Sorgen PL. Secondary structural analysis of the carboxyl-terminal domain from different connexin isoforms. Biopolymers. 2016 Mar; 105 (3): 143-62. PMID: 26542351.

Stauch KL, Purnell PR, Villeneuve LM, and Fox HS. Data for mitochondrial proteomic alterations in the aging mouse brain. Data Brief. 2015 May 21; 4: 127-9. PMID: 26217775.

Villeneuve LM, Stauch KL, and Fox HS. Data for mitochondrial proteomic alterations in the developing rat brain. Data Brief. 2014 Aug 12; 1: 42-5. PMID: 26217684.

Stauch KL, Purnell PR, Villeneuve LM, and Fox HS. Proteomic analysis and functional characterization of mouse brain mitochondria during aging reveal alterations in energy metabolism. Proteomics. 2015 May; 15 (9): 1574-86. PMID: 25546256.

Villeneuve LM, Stauch KL, and Fox HS. Proteomic analysis of the mitochondria from embryonic and postnatal rat brains reveals response to developmental changes in energy demands. J Proteomics. 2014 Sep 23; 109: 228-39. PMID: 25046836.

Stauch KL, Purnell PR, and Fox HS. Aging synaptic mitochondria exhibit dynamic proteomic changes while maintaining bioenergetic function. Aging. 2014 Apr; 6 (4): 320-34. PMID: 24827396.

Stauch KL, Purnell PR, Fox HS. Quantitative proteomics of synaptic and nonsynaptic mitochondria: insights for synaptic mitochondrial vulnerability. J Proteome Res. 2014 May 2; 13 (5): 2620-36. PMID: 24708184.

Stauch K, Kieken F, and Sorgen P. Characterization of the structure and intermolecular interactions between the connexin 32 carboxyl-terminal domain and the protein partners synapse-associated protein 97 and calmodulin. J Biol Chem. 2012 Aug 10; 287 (33): 27771-88. PMID: 22718765.

Kieken F, Mutsaers N, Dolmatova E, Virgil K, Wit AL, Kellezi A, Hirst-Jensen BJ, Duffy HS, and Sorgen PL. Structural and molecular mechanisms of gap junction remodeling in epicardial border zone myocytes following myocardial infarction. Circ Res. 2009 May 8; 104 (9): 1103-12. PMID: 19342602.

Additional publications in PubMed.

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