Some metabolic disorders, such as type 2 diabetes mellitus (T2DM) are risk factors for the development of cognitive deficits and Alzheimer's disease (AD). Epidemiological studies suggest that in people with T2DM, the risk of developing dementia is 2.5 times higher than that in the non-diabetic population. The signaling pathways that underlie the increased risk and facilitate cognitive deficits are not fully understood. In fact, the cause of memory deficits in AD is not fully elucidated. The dentate gyrus of the hippocampus plays an important role in memory formation. Hippocampal neurogenesis is the generation of new neurons and glia in the adult brain throughout life. New neurons incorporate in the granular cell layer of the dentate gyrus and play a role in learning and memory and hippocampal plasticity. A large body of studies suggests that hippocampal neurogenesis is impaired in mouse models of AD and T2DM. Recent evidence shows that hippocampal neurogenesis is also impaired in human patients exhibiting mild cognitive impairment or AD. This review discusses the role of hippocampal neurogenesis in the development of cognitive deficits and AD, and considers inflammatory and endothelial signaling pathways in T2DM that may compromise hippocampal neurogenesis and cognitive function, leading to AD.
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http://dx.doi.org/10.1016/bs.irn.2020.03.020 | DOI Listing |
J Ethnopharmacol
March 2025
Interdisciplinary Institute for Personalized Medicine in Brain Disorders, Jinan University, School of Chinese medicine, Guangzhou, 510632, China; f GHM Joint Laboratory of Traditional Chinese Medicine on Brain-Peripheral Homeostasis and Comprehensive Health, Jinan University, School of Chinese medicine, Guangzhou, 510632, China; Zhuhai Institute of Jinan University, Zhuhai, 519070, China. Electronic address:
Ethnopharmacological Relevancy: Lancao decoction (LC) is a traditional Chinese medicine (TCM) formulation mentioned in the "Huangdineijing", known for its ability to dispel turbidity and eliminate heat. TCM believes that the etiology of Alzheimer's disease (AD) is phlegm turbidity, and the fiery internal obstruction of the gods, which suggests that LC has the possibility of treating.
Aim Of The Study: This investigation will examine the possibilities of LC to improve AD and uncover the underlying mechanisms.
eNeuro
March 2025
Michael Smith Laboratories, University of British Columbia. 2185 East Mall. Vancouver, B.C., V6T 1Z4, Canada.
T-type calcium channels shape neuronal excitability driving burst firing, plasticity and neuronal oscillations that influence circuit activity. The three biophysically distinct T-type channel subtypes (Cav3.1, Cav3.
View Article and Find Full Text PDFMethods Mol Biol
March 2025
The Neurogenesis, Neuroinflammation and Network Dynamics Lab (3ND), Achucarro Basque Center for Neuroscience, Leioa, Spain.
Cultured organotypic hippocampal slices (hOTCs) have become increasingly popular as a model for studying brain function. This model offers significant advantages over traditional in vitro methods, as they allow the examination of mid to long-term manipulations while preserving the structure of the dentate gyrus (DG) in the hippocampus. In this chapter, we focus on a protocol based on hOTCs of mouse entorhinal cortex and hippocampus, which by integrating techniques such as retroviral injections, immunohistochemistry, and microscopy imaging, physiological or pathological processes can be easily investigated.
View Article and Find Full Text PDFMethods Mol Biol
March 2025
Departamento de Fisiología, Facultad de Medicina, Universidad Complutense, Madrid, Spain.
Whole-cell patch clamp allows the evaluation of neuronal excitability and characterization of synaptic transmission. With this technique, it is possible to characterize the neuron maturation level and its integration into the hippocampal circuit. This facilitates the identification of the different stages of neural progenitor cells in the adult brain and their contribution to hippocampal function.
View Article and Find Full Text PDFMethods Mol Biol
March 2025
Univ Lyon, Université Claude Bernard Lyon 1, INSERM, Stem Cell and Brain Research Institute U1208, Bron, France.
Lineage reprogramming of glial cells into induced neurons (iNs) has emerged as an innovative strategy to replace neurons lost due to injury or neurological diseases. Here, we describe a step-by-step protocol to induce in vivo conversion of reactive glial cells, proliferating within the injured hippocampus, into mature and functional GABAergic iNs through retrovirus-mediated expression of two neurogenic fate determinants (Ascl1 and Dlx2). We have previously applied this method to study the integration and functional impact of GABAergic iNs in epileptic mice (Lentini et al.
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