The development of synthetic small molecules capable of promoting neuronal fate in stem cells is a promising strategy to prevent the decline of hippocampal function caused by several neurological disorders. Within this context, isoxazole 9 (Isx-9) has been shown to strongly induce cell proliferation and neuronal differentiation in the subgranular zone (SGZ) of the hippocampal dentate gyrus (DG), while also improving hippocampal function in healthy mice. We have recently demonstrated that Isx-9 is able to restore normal neurogenesis levels after procedural stress. Here, we further discuss these findings highlighting the importance of including a naïve group in studies investigating the effects of either restraint stress or mild chronic unpredictable stress (CUS) on adult hippocampal neurogenesis.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5477711 | PMC |
http://dx.doi.org/10.1080/23262133.2017.1317692 | DOI Listing |
Nat Commun
January 2025
Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
Identifying cell types and brain regions critical for psychiatric disorders and brain traits is essential for targeted neurobiological research. By integrating genomic insights from genome-wide association studies with a comprehensive single-cell transcriptomic atlas of the adult human brain, we prioritized specific neuronal clusters significantly enriched for the SNP-heritabilities for schizophrenia, bipolar disorder, and major depressive disorder along with intelligence, education, and neuroticism. Extrapolation of cell-type results to brain regions reveals the whole-brain impact of schizophrenia genetic risk, with subregions in the hippocampus and amygdala exhibiting the most significant enrichment of SNP-heritability.
View Article and Find Full Text PDFNeuromolecular Med
December 2024
Key Laboratory of Physical Fitness and Exercise Rehabilitation of Hunan Province, College of Physical Education, Hunan Normal University, Changsha, 410012, China.
Alzheimer's disease (AD) is the most common neurodegenerative disorder. The neuropathology of AD appears in the hippocampus. The purpose of this work was to reveal key differentially expressed genes (DEGs) in the hippocampus of AD patients and healthy individuals.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Laboratory for Neuropathology, KU Leuven, Leuven, Belgium.
Background: In 43-63% of symptomatic Alzheimer's disease (AD) patients, there is an observed accumulation of misfolded alpha-synuclein (αSyn). Two primary αSyn subtypes have been identified based on the underlying spreading pattern of this pathology: caudo-rostral and amygdala-predominant. Interactions between pathological TDP-43, Tau, and αSyn can aggravate their spread and aggregation.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
The Second Affiliated Hospital of Chongqing Medical University, Chongqing, Chong Qing, China.
Background: Alzheimer's disease (AD) frequently coexists with cerebral small vessel disease (CSVD) is common in the aging population, yet the underlying mechanisms are not yet fully understood. Both long-term blood pressure variability (BPV) and plasma neurofilament light (PNFL) were identified as potential biomarkers for AD and CSVD. This study aims to understand the mechanisms of comorbidity between AD and CSVD by investigating the associations among BPV, PNFL, and comorbidity.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
College of Public Health, University of Kentucky, Lexington, KY, USA.
Background: Brain arteriolosclerosis (B-ASC) is a pathologic hallmark characterized by dysmorphic brain arteriolar wall thickening. B-ASC is a common finding at autopsy in aged persons - some degree of B-ASC is seen in >80% of brains beyond age 80 years - and is associated with cognitive impairment. Hypertension and diabetes are widely recognized as risk factors for B-ASC.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!