Tauopathy is a concept to describe different genetic or metabolic dysfunctions of tau proteins that generate most of the known dementing disorders. Tauopathy is a degenerating process that also affects the entorhinal formation, and then the hippocampal formation in ageing. In Alzheimer's disease (AD), a disease due to APP dysfunction, a similar tauopathy process in observed in neocortical areas, well correlated to cognitive impairment. One important gap of knowledge is the relationship between tauopathy in the hippocampal formation, ageing, AD, and cognitive impairment. Here we show that the multidisciplinary analysis of numerous brains from non-demented and demented patients suggests the following observations: tauopathy of the hippocampal formation in humans is age-related but not an age-dependent process, also independent of AD, but amplified by APP dysfunctions. Tauopathy in the entorhinal and hippocampal formation could be another type of pathological dysfunction of tau proteins, and a therapeutic target to delay AD. Relevant animal models are desperately needed to address this issue.
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http://dx.doi.org/10.1016/s0531-5565(02)00141-9 | DOI Listing |
Acupunct Med
January 2025
Combination of Acupuncture and Medicine Innovation Research Center, Shaanxi University of Chinese Medicine, Xianyang, China.
Objective: Cognitive impairment (CI) is highly prevalent in subarachnoid hemorrhage (SAH) patients. The phosphatidylinositol 3-kinase (PI3K)/AKT pathway plays a critical role in neuronal survival in a variety of central nervous system injuries. This study aimed to determine whether electroacupuncture (EA) at and LI20 ameliorates SAH-CI in a rat model and to examine whether it modulates the PI3K/AKT pathway by administering a PI3K inhibitor (LY294002) versus dimethyl sulfoxide (DMSO) vehicle.
View Article and Find Full Text PDFTheranostics
January 2025
Department of Physiology & Medical Physics, RCSI University of Medicine & Health Sciences, Dublin D02 YN77, Ireland.
Post-traumatic epilepsy (PTE) is one of the most common life-quality reducing consequences of traumatic brain injury (TBI). However, to date there are no pharmacological approaches to predict or to prevent the development of PTE. The P2X7 receptor (P2X7R) is a cationic ATP-dependent membrane channel that is expressed throughout the brain.
View Article and Find Full Text PDFPsychiatry Investig
January 2025
Department of Biomedical Sciences, Center for Glocal Future Biomedical Scientists at Chonnam National University, Gwangju, Republic of Korea.
Objective: This study aims to investigate may moesin deficiency resulted in neurodevelopmental abnormalities caused by negative impact on synaptic signaling ultimately leading to synaptic structure and plasticity.
Methods: Behavioral assessments measured neurodevelopment (surface righting, negative geotaxis, cliff avoidance), anxiety (open field test, elevated plus maze test), and memory (passive avoidance test, Y-maze test) in moesin-knockout mice (KO) compared to wild-type mice (WT). Whole exome sequencing (WES) of brain (KO vs.
Neural Regen Res
January 2025
Department of Molecular and Cellular Biosciences, University of Cincinnati, Cincinnati, OH, USA.
Adult neurogenesis continuously produces new neurons critical for cognitive plasticity in adult rodents. While it is known transforming growth factor-β signaling is important in embryonic neurogenesis, its role in postnatal neurogenesis remains unclear. In this study, to define the precise role of transforming growth factor-β signaling in postnatal neurogenesis at distinct stages of the neurogenic cascade both in vitro and in vivo, we developed two novel inducible and cell type-specific mouse models to specifically silence transforming growth factor-β signaling in neural stem cells in (mGFAPcre-ALK5fl/fl-Ai9) or immature neuroblasts in (DCXcreERT2-ALK5fl/fl-Ai9).
View Article and Find Full Text PDFMol Psychiatry
January 2025
Institut de Neurociències, Department de Bioquímica i Biologia Molecular, Facultat de Medicina, Universitat Autònoma de Barcelona, Bellaterra, Barcelona, Spain.
Alzheimer's disease (AD) is characterized by memory loss and neuropsychiatric symptoms associated with cerebral amyloid-β (Aβ) and tau pathologies, but whether and how these factors differentially disrupt neural circuits remains unclear. Here, we investigated the vulnerability of memory and emotional circuits to Aβ and tau pathologies in mice expressing mutant human amyloid precursor protein (APP), Tau or both APP/Tau in excitatory neurons. APP/Tau mice develop age- and sex-dependent Aβ and phosphorylated tau pathologies, the latter exacerbated at early stages, in vulnerable brain regions.
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