The role of public health versus invasive coronary interventions in the decline of coronary heart disease mortality.

PURPOSE: There has been considerable debate on the extent to which the decline in coronary heart disease (CHD) mortality has been caused by better control of coronary risk factors in the general population or is the result of invasive coronary interventions in symptomatic individuals. METHODS: Using the Myocardial Infarction Data Acquisition System, a statewide database of all cardiovascular hospital admissions in New Jersey, we examined time trends in incidence of death from CHD in the Years 2000-2014 in persons with a history of hospitalization for CHD in the previous 10 years and those without such a history. RESULTS: Over the 10-year study period, there was a marked decline in CHD-related mortality in both persons with a history of CHD and persons without a history of CHD. The decline occurred across all gender, racial, and age groups and was higher in those without a prior history of CHD. CONCLUSIONS: This adds more evidence that the decline in CHD was not only because of advanced invasive medical and surgical treatments but also equally because of improved lifestyle, pharmacologic treatment of risk factors for CHD, and public health interventions.

The role of inflammation in Alzheimer's disease.

Considerable evidence gained over the past decade has supported the conclusion that neuroinflammation is associated with Alzheimer's disease (AD) pathology. Inflammatory components related to AD neuroinflammation include brain cells such as microglia and astrocytes, the classic and alternate pathways of the complement system, the pentraxin acute-phase proteins, neuronal-type nicotinic acetylcholine receptors (AChRs), peroxisomal proliferators-activated receptors (PPARs), as well as cytokines and chemokines. Both the microglia and astrocytes have been shown to generate beta-amyloid protein (Abeta), one of the main pathologic features of AD. Abeta itself has been shown to act as a pro-inflammatory agent causing the activation of many of the inflammatory components. Further substantiation for the role of neuroinflammation in AD has come from studies that demonstrate patients who took non-steroidal anti-inflammatory drugs had a lower risk of AD than those who did not. These same results have led to increased interest in pursuing anti-inflammatory therapy for AD but with poor results. On the other hand, increasing amount of data suggest that AChRs and PPARs are involved in AD-induced neuroinflammation and in this regard, future therapy may focus on their specific targeting in the AD brain.