Search PubMedSearch

PubMed · 7710369

Stroke prevention.

Abstract

Stroke is ideally suited for prevention. It has a high prevalence, burden of illness, and economic cost, and safe and effective prevention measures. The estimated $30 billion that is being spent for stroke each year in the United States should not come as a surprise given the approximately 3 million stroke survivors and 400,000 to 500,000 new or recurrent stroke cases annually. Stroke remains the third leading cause of death among adults and has been targeted for cost containment by managed care health systems and other insurers. The US Public Health Service in conjunction with the National Health Promotion and Disease Prevention Objectives has set a goal to reduce stroke deaths to 20 per 100,000 by the year 2000. This goal could be attained as the estimate of "preventable" strokes could be as high as 80%. In this article, I will review the status of stroke risk factors, prevention approaches to reduce stroke, clinical trial data from primary and secondary stroke prevention studies, and future directions in stroke prevention.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

P B Gorelick. 1995. Stroke prevention.. https://doi.org/10.1001/archneur.1995.00540280029015

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

FGF21 suppresses alcohol consumption through an amygdalo-striatal circuit.

Excessive alcohol consumption is a major health and social issue in our society. Pharmacologic administration of the endocrine hormone fibroblast growth factor 21 (FGF21) suppresses alcohol consumption through actions in the brain in rodents, and genome-wide association studies have identified single nucleotide polymorphisms in genes involved with FGF21 signaling as being associated with increased alcohol consumption in humans. However, the neural circuit(s) through which FGF21 signals to suppress alcohol consumption are unknown, as are its effects on alcohol consumption in higher organisms. Here, we demonstrate that administration of an FGF21 analog to alcohol-preferring non-human primates reduces alcohol intake by 50%. Further, we reveal that FGF21 suppresses alcohol consumption through a projection-specific subpopulation of KLB-expressing neurons in the basolateral amygdala. Our results illustrate how FGF21 suppresses alcohol consumption through a specific population of neurons in the brain and demonstrate its therapeutic potential in non-human primate models of excessive alcohol consumption.

Alcohol Drinking