Parkinson’s disease is the second most common neurodegenerative disorder after Alzheimer’s disease affecting approximately1% of the population older than 50 years. There is a worldwide increase in disease prevalence due to the increasing age of human populations. A definitive neuropathological diagnosis of Parkinson’s disease requires loss of dopaminergic neurons in the substantia nigra and related brain stem nuclei, and the presence of Lewy bodies in remaining nerve cells. The contribution of genetic factors to the pathogenesis of Parkinson’s disease is increasingly being recognized. A point mutation which is sufficient to cause a rare autosomal dominant form of the disorder has been recently identified in the α-synuclein gene on chromosome 4 in the much more common sporadic, or ‘idiopathic’ form of Parkinson’s disease, and a defect of complex I of the mitochondrial respiratory chain was confirmed at the biochemical level. Disease specificity of this defect has been demonstrated for the parkinsonian substantia nigra. These findings and the observation that the neurotoxin 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP), which causes a Parkinson-like syndrome in humans, acts via inhibition of complex I have triggered research interest in the mitochondrial genetics of Parkinson’s disease. Oxidative phosphorylation consists of five protein-lipid enzyme complexes located in the mitochondrial inner membrane that contain flavins (FMN, FAD), quinoid compounds (coenzyme Q₁₀, CoQ₁₀) and transition metal compounds (iron-sulfur clusters, hemes, protein-bound copper). These enzymes are designated complex I (NADH:ubiquinone oxidoreductase, EC 1.6. 5.3), complex II (succinate:ubiquinone oxidoreductase, EC 1.3.5.1), complex III (ubiquinol:ferrocytochrome c oxidoreductase, EC 1.10.2.2), complex IV (ferrocytochrome c:oxygen oxidoreductase or cytochrome c oxidase, EC 1.9.3.1), and complex V (ATP synthase, EC 3.6.1.34). A defect in mitochondrial oxidative phosphorylation, in terms of a reduction in the activity of NADH CoQ reductase (complex I) has been reported in the striatum of patients with Parkinson’s disease. The reduction in the activity of complex I is found in the substantia nigra, but not in other areas of the brain, such as globus pallidus or cerebral cortex. Therefore, the specificity of mitochondrial impairment may play a role in the degeneration of nigrostriatal dopaminergic neurons. This view is supported by the fact that MPTP generating 1-methyl-4-phenylpyridine (MPP⁺) destroys dopaminergic neurons in the substantia nigra. Although the serum levels of CoQ₁₀ is normal in patients with Parkinson’s disease, CoQ₁₀ is able to attenuate the MPTP-induced loss of striatal dopaminergic neurons.

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Despite decades of public health initiatives, tobacco use remains the leading known preventable cause of death in the United States. Clinicians have a proven, positive effect on patients' ability to quit, and pharmacists are strategically positioned to assist patients with quitting. The American Association of Colleges of Pharmacy recognizes health promotion and disease prevention as a key educational outcome; as such, tobacco cessation education should be a required component of pharmacy curricula to ensure that all pharmacy graduates possess the requisite evidence-based knowledge and skills to intervene with patients who use tobacco. Faculty members teaching tobacco cessation-related content must be knowledgeable and proficient in providing comprehensive cessation counseling, and all preceptors and practicing pharmacists providing direct patient care should screen for tobacco use and provide at least minimal counseling as a routine component of care. Pharmacy organizations should establish policies and resolutions addressing the profession's role in tobacco cessation and control, and the profession should work together to eliminate tobacco sales in all practice settings where pharmacy services are rendered.

Objective. To determine first-year pharmacy students' analysis, confidence, and knowledge of patient physical assessment integrated within a pathophysiology curriculum. Design. A prospective quasi-experimental study using validated pre-and post-surveys and follow-up examinations was conducted to objectively assess the confidence and knowledge of pharmacy students' physical assessment skills. Assessment. Students' perceived ability to perform physical assessment techniques improved. Topic mastery was demonstrated by a final comprehensive examination with a composite student class score of 83%. Conclusion. First-year pharmacy students demonstrated acquisition of patient physical assessment skills when integrated into a pathophysiology course.