Browsing by Subject "Neuropathology"

Now showing 1 - 3 of 3
  • Thumbnail Image
    Publication
    Open Access
    Alzheimer ß-amyloid peptides normal and abnormal localization
    (Murcia : F. Hernández, 2002) Takahashi, R.H.; Nam, E.E.; Edgar, M.; Gouras, G.K.
    Alzheimer's disease (AD) neuropathology is characterized by accumulation of “senile” plaques (SPs) and neurofibrillary tangles (NFTs) in vulnerable brain regions. SPs are principally composed of aggregates of up to 42/43 amino acid ß-amyloid (Aß) peptides. The discovery of familial AD (FAD) mutations in the genes for the amyloid precursor protein (APP) and presenilins (PSs), all of which increase Aß42 production, support the view that Aß is centrally involved in the pathogenesis of AD. Aß42 aggregates readily, and is thought to seed the formation of fibrils, which then act as templates for plaque formation. Aß is generated by the sequential intracellular cleavage of APP by ßsecretase to generate the N-terminal end of Aß, and intramembranous cleavage by g-secretase to generate the C-terminal end. Cell biological studies have demonstrated that Aß is generated in the ER, Golgi, and endosomal/lysosomal system. A central question involving the role of Aß in AD concerns how Aß causes disease and whether it is extracellular Aß deposition and/or intracellular Aß accumulation that initiates the disease process. The most prevalent view is that SPs are composed of extracellular deposits of secreted Aß and that Aß causes toxicity to surrounding neurons as extracellular SP. The recent emphasis on the intracellular biology of APP and Aß has led some investigators to consider the possibility that intraneuronal Aß may directly cause toxicity. In this review we will outline current knowledge of the localization of both intracellular and extracellular Aß.
  • Thumbnail Image
    Item
    Open Access
    NeuN expression in health and disease: A histological perspective on neuronal heterogeneity
    (Universidad de Murcia, Departamento de Histología e Histopatología, 2026) Moon, Joongbum; Hyeon Ahn, Ji; Won, Moo-Ho; Biología Celular e Histología
    Neuronal nuclei (NeuN), also known as Rbfox3, is a widely used neuronal marker for identifying postmitotic neurons in both basic neuroscience and diagnostic neuropathology. Since its discovery, NeuN immunoreactivity has enabled accurate neuron counting, injury assessment, and anatomical mapping. However, accumulating evidence demonstrates that NeuN is not universally expressed across all mature neurons. Specific neuron types, such as olfactory mitral cells, cerebellar Purkinje cells, and retinal photoreceptors, consistently lack NeuN immunostaining despite functional maturity. Moreover, NeuN expression is dynamically regulated under pathological conditions. In ischemia-reperfusion (I/R) injury, neurodegenerative diseases (e.g., Alzheimer’s and Parkinson’s), and traumatic brain injury or epilepsy, selected for their representative diversity in pathophysiological stress (ischemic, degenerative, and mechanical), NeuN downregulation may reflect functional compromise, stress responses, or reversible transcriptional changes rather than irreversible cell loss. These findings highlight the limitations of interpreting NeuN negativity as neuronal death. This review synthesizes recent findings on NeuN expression patterns, molecular mechanisms regulating its presence or absence, and the implications for research and diagnosis. We propose that NeuN should not be regarded as a binary marker but rather as a dynamic indicator of neuronal state. Multi-marker strategies and molecular tools such as spatial transcriptomics and RNA sequencing are suggested to improve the resolution of neuronal analysis. As histological and transcriptomic approaches converge, NeuN’s role will likely expand from a structural identifier to a contextual readout of neuronal integrity and function.
  • Thumbnail Image
    Publication
    Open Access
    Pathomechanism of entrapment neuropathy in diabetic and nondiabetic rats reared in wire cages
    (Murcia : F. Hernández, 2008) Nishimura, Toshico; Hirata, Hitoshi; Tsujil, Masaya; Iida, Ryu; Hoki, Yoko; Iino, Takahiro; Ogawa, Satoru; Uchida, Atsumasa
    To examine the pathomechanism of entrapment neuropathy associated with diabetes with special emphasis on the roles of mast cells and Tenascin- C using a rat model of Streptozotocin-induced diabetes. The roles of mast cells and Tenascin-C in development of tarsal tunnel syndrome were analyzed electrophysiologically and histologically in 20 male Ws/Ws-/-rats (mast cell deficient) and 20 of their male wild type counterparts (12-16 weeks old; 250-300g). Rats were assigned randomly to one of the following three groups; diabetic group and nondiabetic group reared in cages with a wire grid flooring; non-diabetic group in cages with sawdust covered plastic flooring. No significant role for mast cells in entrapment neuropathy was found in the rats with streptozotocin-induced diabetes. Distal latency was prolonged in diabetic rats compared with nondiabetic rats, and positively correlated with increases in blood glucose levels. Tenascin-C expression levels in the endoneurium at the tarsal tunnel in diabetic rats were found to be correlated with distal latency. The anti-alpha-smooth muscle actin (a-SMA) positive myofibroblast was scattered in nerve fascicles overexpressing Tenascin-C. It seems likely that Tenascin-C expressing myofibroblasts constrict axons by inducing collagen contraction of the endoneurium. Our data indicate that metabolic and phenotypic abnormalities of endoneurium and perineurum lie behind the vulnerability of diabetic patients to entrapment neuropathy.