Twenty-five years of progress: the view from NIMH and NINDS.

Neuron

National Institute of Mental Health, 6001 Executive Boulevard, Room 8129, MSC 9669, Bethesda, MD 20892-9669, USA. Electronic address:

Published: October 2013

As directors of two NIH institutes supporting neuroscience research, we explore the gap between 25 years of stunning progress in fundamental neuroscience and the persistent needs of those with brain disorders. We conclude that closing this gap will require a more detailed comprehension of brain function, a rethinking of how we approach translational science, a focus on human neurobiology, and a continuing commitment to build a diverse, innovative neuroscience workforce. In contrast to many other areas of medicine, we lack basic knowledge about our organ of interest. The next phase of progress on brain disorders will require a significantly deeper understanding of fundamental neurobiology.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3859529PMC
http://dx.doi.org/10.1016/j.neuron.2013.09.041DOI Listing

Publication Analysis

Top Keywords

brain disorders
8
will require
8
twenty-five years
4
years progress
4
progress view
4
view nimh
4
nimh ninds
4
ninds directors
4
directors nih
4
nih institutes
4

Similar Publications

Background & Aims: Hepatic encephalopathy (HE), one of the most serious prognostic factors for mortality in alcohol-related cirrhosis (ALD cirrhosis), is not recorded in Danish healthcare registries. However, treatment of HE with lactulose, the universal first-line treatment, can be identified through data on filled prescriptions. This study aimed to investigate if lactulose can be used as a surrogate marker of HE.

View Article and Find Full Text PDF

L-carnitine protects against oxidative damage and neuroinflammation in cerebral cortex of rats submitted to chronic chemically-induced model of hyperphenylalaninemia.

Metab Brain Dis

January 2025

Programa de Pós-Graduação em Ciências Farmacêuticas, Universidade Federal do Rio Grande do Sul, Avenida Ipiranga, 2752, Porto Alegre, CEP 90610-000, RS, Brazil.

Phenylketonuria is a genetic disorder characterized by high phenylalanine levels, the main toxic metabolite of the disease. Hyperphenylalaninemia can cause neurological impairment. In order to avoid this symptomatology, patients typically follow a phenylalanine-free diet supplemented with a synthetic formula that provides essential amino acids, including L-carnitine.

View Article and Find Full Text PDF

Modulation of Intestinal Inflammation and Protection of Dopaminergic Neurons in Parkinson's Disease Mice through a Probiotic Formulation Targeting NLRP3 Inflammasome.

J Neuroimmune Pharmacol

January 2025

Laboratory Medicine Center, Department of Clinical Laboratory, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, PR China.

Emerging evidence highlights the significance of peripheral inflammation in the pathogenesis of Parkinson's disease (PD) and suggests the gut as a viable therapeutic target. This study aimed to explore the neuroprotective effects of the probiotic formulation VSL#3 and its underlying mechanism in a PD mouse model induced by MPTP. Following MPTP administration, the striatal levels of dopamine and its metabolites, as along with the survival rate of dopaminergic neurons in the substantia nigra, were significantly reduced in PD mice.

View Article and Find Full Text PDF

Minimally invasive parafascicular surgery (MIPS) with the use of tubular retractors achieve a safe resection in deep seated tumours. Diffusion changes noted on postoperative imaging; the significance and clinical correlation of this remains poorly understood. Single centre retrospective cohort study of neuro-oncology patients undergoing MIPS.

View Article and Find Full Text PDF

Progress report on multiple endocrine neoplasia type 1.

Fam Cancer

January 2025

Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.

Multiple endocrine neoplasia type 1 (MEN1) syndrome is an autosomal dominant disorder caused by a germline pathogenic variant in the MEN1 tumor suppressor gene. Patients with MEN1 have a high risk for primary hyperparathyroidism (PHPT) with a penetrance of nearly 100%, pituitary adenomas (PitAd) in 40% of patients, and neuroendocrine neoplasms (NEN) of the pancreas (40% of patients), duodenum, lung, and thymus. Increased MEN1-related mortality is mainly related to duodenal-pancreatic and thymic NEN.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!