Next Article in Journal
Spironolactone Plus Full-Dose ACE Inhibition in Patients with Idiopathic Membranous Nephropathy and Nephrotic Syndrome: Does It Really Work?
Next Article in Special Issue
Oxidative Stress Induced Mitochondrial Failure and Vascular Hypoperfusion as a Key Initiator for the Development of Alzheimer Disease
Previous Article in Journal / Special Issue
Insulin and Insulin-Sensitizing Drugs in Neurodegeneration: Mitochondria as Therapeutic Targets

Mitochondrial Drugs for Alzheimer Disease

Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
Memory and Cognition Center, University Hospitals Case Medical Center, Beachwood, OH 44122, USA
Department of Neurodegenerative Diseases, Institute of Agricultural Medicine, Lublin, Poland
UTSA Neurosciences Institute and Department of Biology, College of Sciences, University of Texas at San Antonio, San Antonio, TX 78249, USA
Author to whom correspondence should be addressed.
Pharmaceuticals 2009, 2(3), 287-298;
Received: 23 October 2009 / Revised: 14 December 2009 / Accepted: 16 December 2009 / Published: 23 December 2009
(This article belongs to the Special Issue Mitochondrial Drugs for Neurodegenerative Diseases)
Therapeutic strategies for Alzheimer disease (AD) have yet to offer a diseasemodifying effect to stop the debilitating progression of neurodegeneration and cognitive decline. Rather, treatments thus far are limited to agents that slow disease progression without halting it, and although much work towards a cure is underway, a greater understanding of disease etiology is certainly necessary for any such achievement. Mitochondria, as the centers of cellular metabolic activity and the primary generators of reactive oxidative species in the cell, received particular attention especially given that mitochondrial defects are known to contribute to cellular damage. Furthermore, as oxidative stress has come to the forefront of AD as a causal theory, and as mitochondrial damage is known to precede much of the hallmark pathologies of AD, it seems increasingly apparent that this metabolic organelle is ultimately responsible for much, if not all of disease pathogenesis. In this review, we review the role of neuronal mitochondria in the pathogenesis of AD and critically assess treatment strategies that utilize this upstream access point as a method for disease prevention. We suspect that, with a revived focus on mitochondrial repair and protection, an effective and realistic therapeutic agent can be successfully developed. View Full-Text
Keywords: Alzheimer disease; antioxidant; coenzyme Q; Dimebon; fission; fusion; mitochondria; mitochondrial drugs; mitochondrial permeability transition pore; oxidative stress Alzheimer disease; antioxidant; coenzyme Q; Dimebon; fission; fusion; mitochondria; mitochondrial drugs; mitochondrial permeability transition pore; oxidative stress
Show Figures

Graphical abstract

MDPI and ACS Style

Bonda, D.J.; Wang, X.; Gustaw-Rothenberg, K.A.; Perry, G.; Smith, M.A.; Zhu, X. Mitochondrial Drugs for Alzheimer Disease. Pharmaceuticals 2009, 2, 287-298.

AMA Style

Bonda DJ, Wang X, Gustaw-Rothenberg KA, Perry G, Smith MA, Zhu X. Mitochondrial Drugs for Alzheimer Disease. Pharmaceuticals. 2009; 2(3):287-298.

Chicago/Turabian Style

Bonda, David J., Xinglong Wang, Katarzyna A. Gustaw-Rothenberg, George Perry, Mark A. Smith, and Xiongwei Zhu. 2009. "Mitochondrial Drugs for Alzheimer Disease" Pharmaceuticals 2, no. 3: 287-298.

Find Other Styles

Article Access Map by Country/Region

Only visits after 24 November 2015 are recorded.
Back to TopTop