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Journal articles on the topic 'Neuronal ageing'

Author: Grafiati

Published: 4 June 2025

Last updated: 1 August 2025

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1

Mattson, Mark P., and Tim Magnus. "Ageing and neuronal vulnerability." Nature Reviews Neuroscience 7, no. 4 (2006): 278–94. http://dx.doi.org/10.1038/nrn1886.

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2

Verkhratsky, Alexej, and Emil C. Toescu. "Calcium and neuronal ageing." Trends in Neurosciences 21, no. 1 (1998): 2–7. http://dx.doi.org/10.1016/s0166-2236(97)01156-9.

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3

Toescu, Emil. "The healthy ageing of the Ca2+ hypothesis." Ageing & Longevity, no. 1.2025 (February 11, 2025): 37–45. https://doi.org/10.47855/jal9020-2025-1-5.

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Normal brain ageing is associated with a varying degree of cognitive impairment. One of the early hypotheses proposed to explain such changes was the “Ca2+ hypothesis of ageing”. This review revisits this hypothesis and uses the Ca2+ dependency of neuronal excitability as an integrator to discuss the age-dependent changes in the activity of the various systems and mechanisms that control neuronal Ca2+ homeostasis. Amongst these systems, special attention is given to the mitochondrial involvement in the regulation of neuronal Ca2+, and to the fact that changes in mitochondrial functions induced

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4

Tsvetanov, Kamen A., Richard N. A. Henson, and James B. Rowe. "Separating vascular and neuronal effects of age on fMRI BOLD signals." Philosophical Transactions of the Royal Society B: Biological Sciences 376, no. 1815 (2020): 20190631. http://dx.doi.org/10.1098/rstb.2019.0631.

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Accurate identification of brain function is necessary to understand the neurobiology of cognitive ageing, and thereby promote well-being across the lifespan. A common tool used to investigate neurocognitive ageing is functional magnetic resonance imaging (fMRI). However, although fMRI data are often interpreted in terms of neuronal activity, the blood oxygenation level-dependent (BOLD) signal measured by fMRI includes contributions of both vascular and neuronal factors, which change differentially with age. While some studies investigate vascular ageing factors, the results of these studies a

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5

Toescu, Emil C., and Alex Verkhratsky. "Neuronal ageing in long-term cultures." NeuroReport 11, no. 17 (2000): 3725–29. http://dx.doi.org/10.1097/00001756-200011270-00027.

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6

Okenve-Ramos, Pilar, Rory Gosling, Monika Chojnowska-Monga, et al. "Neuronal ageing is promoted by the decay of the microtubule cytoskeleton." PLOS Biology 22, no. 3 (2024): e3002504. http://dx.doi.org/10.1371/journal.pbio.3002504.

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Natural ageing is accompanied by a decline in motor, sensory, and cognitive functions, all impacting quality of life. Ageing is also the predominant risk factor for many neurodegenerative diseases, including Parkinson’s disease and Alzheimer’s disease. We need to therefore gain a better understanding of the cellular and physiological processes underlying age-related neuronal decay. However, gaining this understanding is a slow process due to the large amount of time required to age mammalian or vertebrate animal models. Here, we introduce a new cellular model within the Drosophila brain, in wh

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Sharma, S. P., I. K. Patro, Nisha Patro, and T. J. James. "‘Dark’ type Purkinje cells and neuronal ageing." Proceedings: Animal Sciences 97, no. 5 (1988): 449–53. http://dx.doi.org/10.1007/bf03179952.

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8

Delgado‐González, José Carlos, Carlos Rosa‐Prieto, Diana Lucía Tarruella‐Hernández, et al. "Neuronal volume of the hippocampal regions in ageing." Journal of Anatomy 237, no. 2 (2020): 301–10. http://dx.doi.org/10.1111/joa.13189.

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9

TOESCU, EMIL C., and ALEXEJ VERKHRATSKY. "Parameters of calcium homeostasis in normal neuronal ageing." Journal of Anatomy 197, no. 4 (2000): 563–69. http://dx.doi.org/10.1046/j.1469-7580.2000.19740563.x.

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10

Surmeier, D. James. "Calcium, ageing, and neuronal vulnerability in Parkinson's disease." Lancet Neurology 6, no. 10 (2007): 933–38. http://dx.doi.org/10.1016/s1474-4422(07)70246-6.

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11

Mack, Till Georg Alexander, Patricia Kreis, and Britta Johanna Eickholt. "Defective actin dynamics in dendritic spines: cause or consequence of age-induced cognitive decline?" Biological Chemistry 397, no. 3 (2016): 223–29. http://dx.doi.org/10.1515/hsz-2015-0185.

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Abstract Ageing is a complex deteriorating process that coincides with changes in metabolism, replicative senescence, increased resistance to apoptosis, as well as progressive mitochondria dysfunction that lead to an increase production and accumulation of reactive oxygen species (ROS). Although controversy on the paradigm of the oxidative damage theory of ageing exists, persuasive studies in Caenorhabditis elegans and yeast have demonstrated that manipulation of ROS can modify the process of ageing and influences the damage of proteins, lipids and DNA. In neurons, ageing impacts on the intrin

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12

Toescu, Emil C. "Normal brain ageing: models and mechanisms." Philosophical Transactions of the Royal Society B: Biological Sciences 360, no. 1464 (2005): 2347–54. http://dx.doi.org/10.1098/rstb.2005.1771.

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Normal ageing is associated with a degree of decline in a number of cognitive functions. Apart from the issues raised by the current attempts to expand the lifespan, understanding the mechanisms and the detailed metabolic interactions involved in the process of normal neuronal ageing continues to be a challenge. One model, supported by a significant amount of experimental evidence, views the cellular ageing as a metabolic state characterized by an altered function of the metabolic triad: mitochondria–reactive oxygen species (ROS)–intracellular Ca 2+ . The perturbation in the relationship betwe

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13

Farina, Sofia, Alessandro Cattabiani, Darshan Mandge, et al. "A multiscale electro-metabolic model of a rat neocortical circuit reveals the impact of ageing on central cortical layers." PLOS Computational Biology 21, no. 5 (2025): e1013070. https://doi.org/10.1371/journal.pcbi.1013070.

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The high energetic demands of the brain arise primarily from neuronal activity. Neurons consume substantial energy to transmit information as electrical signals and maintain their resting membrane potential. These energetic requirements are met by the neuro-glial-vascular (NGV) ensemble, which generates energy in a coupled metabolic process. In ageing, metabolic function becomes impaired, producing less energy and, consequently, the system is unable to sustain the neuronal energetic needs. We propose a multiscale model of electro-metabolic coupling in a reconstructed rat neocortex. This combin

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14

Guertin, PA. "Could Ageing-Related Chronic Skin Problems be Attributed to Neuronal and Non-Neuronal Dysfunctions?" Archive of Gerontology and Geriatrics Research 1, no. 1 (2016): 001–2. http://dx.doi.org/10.17352/aggr.000001.

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15

Markaki, Maria, Dikaia Tsagkari, and Nektarios Tavernarakis. "Mitophagy mechanisms in neuronal physiology and pathology during ageing." Biophysical Reviews 13, no. 6 (2021): 955–65. http://dx.doi.org/10.1007/s12551-021-00894-7.

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16

Foster, Thomas C., and Christopher M. Norris. "Calcium and Neuronal Ageing.: Comment on Verkhratsky et al." Trends in Neurosciences 21, no. 7 (1998): 286–87. http://dx.doi.org/10.1016/s0166-2236(98)01259-4.

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17

Yanti, V. N. A. Maha, D. Subali, and R. R. Tjandrawinata. "Functional efficacy of tempeh oil microemulsion containing omega 3 for Alzheimer’s protection." Food Research 7, no. 6 (2023): 168–76. http://dx.doi.org/10.26656/fr.2017.7(6).977.

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Alzheimer’s disease (AD) is associated with ageing symptoms due to stress oxidative, neuroinflammation, acetylcholinesterase and butyrylcholinesterase activation, and Tau hyperphosphorylation. Tempeh has been recognized as one of the Indonesian traditional fermented foods made from soybean fermentation with a microbial consortium. Our previous study demonstrated that tempeh oil contains polyunsaturated fatty acids (PUFAs) and antioxidants for ageing prevention. Tempeh oil rich in PUFAs may be developed as a modern functional supplement for AD protection. This study aimed to extract tempeh oil,

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18

Coelho, Joana. "Vitamin D for Neuroprotection and for Alzheimer’s Disease Prevention and Treatment." Progress in Medical Sciences 8, no. 1 (2024): 1–5. http://dx.doi.org/10.47363/pms/2024(8)195.

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19

Shukitt-Hale, Barbara. "Blueberries and Neuronal Aging." Gerontology 58, no. 6 (2012): 518–23. http://dx.doi.org/10.1159/000341101.

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20

Mello, Sônia A., Angélica C. M. Marese, Rose M. C. Brancalhão, Jacqueline N. Zanoni, and Maria Raquel M. Natali. "Administering ascorbic acid to rats undergoing ageing processes: effects on myosin-V immunoreactive myenteric neurons." Anais da Academia Brasileira de Ciências 85, no. 1 (2013): 337–47. http://dx.doi.org/10.1590/s0001-37652013005000002.

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During the ageing process the enteric nervous system undergoes morphofunctional changes, such as enteric neurodegeneration. Neuronal death can be attributed to increase radicals free, and ascorbic acid (AA), known antioxidant, could minimize damage cause by oxidative stress. The objective of this study is to analyse the behaviour of morphoquantative myenteric neurons in the duodenum of adult Wistar rats with aged 90 (C90), 345 (E345) and 428 (E428) days, as well as animals of the same age who received ascorbic acid supplementation for 120 days (EA345 and EA428). Whole-mount preparations of mus

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21

Magrone, Thea, Manrico Magrone, Matteo A. Russo, and Emilio Jirillo. "Peripheral Immunosenescence and Central Neuroinflammation: A Dangerous Liaison - A Dietary Approach." Endocrine, Metabolic & Immune Disorders - Drug Targets 20, no. 9 (2020): 1391–411. http://dx.doi.org/10.2174/1871530320666200406123734.

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Background & Objectives: In old people, both innate and adaptive immune responses are impaired, thus leading to a condition of systemic inflamm-ageing, even including the involvement of the central nervous system (CNS). Aims: Here, main mechanisms of the immune ageing and neuro-inflammation will be discussed along with the dietary approaches for the modulation of age related diseases. Discussion: Neuroinflammation is caused by the passage of inflammatory mediators through the brain blood barrier to CNS. Then, in the brain, antigenic stimulation of microglia and/or its activation by periphe

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22

Yanai, T., T. Masegi, K. Yoshida, et al. "Eosinophilic neuronal inclusions in the thalamus of ageing B6C3F1 mice." Journal of Comparative Pathology 113, no. 3 (1995): 287–90. http://dx.doi.org/10.1016/s0021-9975(05)80043-x.

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23

Ramos, R., V. Requena, F. Díaz, A. Villena, and I. Pérez de Vargas. "Evolution of neuronal density in the ageing thalamic reticular nucleus." Mechanisms of Ageing and Development 83, no. 1 (1995): 21–29. http://dx.doi.org/10.1016/0047-6374(95)01617-9.

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24

Bano, Daniele, Massimiliano Agostini, Gerry Melino, and Pierluigi Nicotera. "Ageing, Neuronal Connectivity and Brain Disorders: An Unsolved Ripple Effect." Molecular Neurobiology 43, no. 2 (2011): 124–30. http://dx.doi.org/10.1007/s12035-011-8164-6.

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25

Szinyákovics, Janka, Fanni Keresztes, Eszter Anna Kiss, Gergő Falcsik, Tibor Vellai, and Tibor Kovács. "Potent New Targets for Autophagy Enhancement to Delay Neuronal Ageing." Cells 12, no. 13 (2023): 1753. http://dx.doi.org/10.3390/cells12131753.

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Autophagy is a lysosomal-dependent degradation process of eukaryotic cells responsible for breaking down unnecessary and damaged intracellular components. Autophagic activity gradually declines with age due to genetic control, and this change contributes to the accumulation of cellular damage at advanced ages, thereby causing cells to lose their functionality and viability. This could be particularly problematic in post-mitotic cells including neurons, the mass destruction of which leads to various neurodegenerative diseases. Here, we aim to uncover new regulatory points where autophagy could

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26

Rossor, M., and C. Q. Mountjoy. "Post-Mortem Neurochemical Changes in Alzheimer's Disease Compared With Normal Ageing." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 13, S4 (1986): 499–502. http://dx.doi.org/10.1017/s0317167100037203.

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Abstract:Selective neuronal degeneration with concomitant changes in neurotransmitter systems are features of both normal ageing and Alzheimer's disease. There are, however, important neurochemical differences in cerebral cortex. Choline acetyltransferase declines with age in frontal cortex in contrast to the prominent change in the temporal cortex in Alzheimer's disease. The loss of somatostatin, and the recently reported reciprocal change in corticotropin-releasing factor and receptors are not seen with ageing. However, age itself may have an important influence on the neurochemical deficits

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27

Peradinovic, Josip, Nikolina Mohovic, Katarina Bulic, Andrea Markovinovic, Raffaello Cimbro, and Ivana Munitic. "Ageing-Induced Decline in Primary Myeloid Cell Phagocytosis Is Unaffected by Optineurin Insufficiency." Biology 12, no. 2 (2023): 240. http://dx.doi.org/10.3390/biology12020240.

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Optineurin is a ubiquitin-binding adaptor protein involved in multiple cellular processes, including innate inflammatory signalling. Mutations in optineurin were found in amyotrophic lateral sclerosis, an adult-onset fatal neurodegenerative disease that targets motor neurons. Neurodegeneration results in generation of neuronal debris, which is primarily cleared by myeloid cells. To assess the role of optineurin in phagocytosis, we performed a flow cytometry-based phagocytic assay of apoptotic neuronal debris and E. coli bioparticles in bone marrow-derived macrophages (BMDMs), and primary neona

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28

TUCKER, M. A., M. F. ANDREW, S. J. OGLE, and J. G. DAVISON. "Age-associated Change in Pain Threshold Measured by Transcutaneous Neuronal Electrical Stimulation." Age and Ageing 18, no. 4 (1989): 241–46. http://dx.doi.org/10.1093/ageing/18.4.241.

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29

Dowson, J. H. "Neuronal Lipopigment: A Marker for Cognitive Impairment and Long-Term Effects of Psychotropic Drugs." British Journal of Psychiatry 155, no. 1 (1989): 1–11. http://dx.doi.org/10.1192/bjp.155.1.1.

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Lipopigment, identifiable in the fluorescence microscope, is thought to be cellular debris partly derived from free-radical-induced peroxidation of cellular constituents. The volume of neuronal lipopigment has been positively correlated with advancing age, Alzheimer dementia, and the neuronal ceroidoses, while various changes in neuronal lipopigment have been reported in association with the chronic administration of dihydroergotoxine, ethanol, phenytoin, centrophenoxine, and chlorpromazine. An increase in the volume of neuronal lipopigment may indicate increased functional activity of the cel

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30

Sinadinos, Christopher, Jordi Valles‐Ortega, Laura Boulan, et al. "Neuronal glycogen synthesis contributes to physiological aging." Aging Cell 13, no. 5 (2014): 935–45. http://dx.doi.org/10.1111/acel.12254.

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31

Verkerke, Marloes, Elly M. Hol, and Jinte Middeldorp. "Physiological and Pathological Ageing of Astrocytes in the Human Brain." Neurochemical Research 46, no. 10 (2021): 2662–75. http://dx.doi.org/10.1007/s11064-021-03256-7.

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AbstractAgeing is the greatest risk factor for dementia, although physiological ageing by itself does not lead to cognitive decline. In addition to ageing, APOE ε4 is genetically the strongest risk factor for Alzheimer’s disease and is highly expressed in astrocytes. There are indications that human astrocytes change with age and upon expression of APOE4. As these glial cells maintain water and ion homeostasis in the brain and regulate neuronal transmission, it is likely that age- and APOE4-related changes in astrocytes have a major impact on brain functioning and play a role in age-related di

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32

Konstantinidis, Georgios, and Nektarios Tavernarakis. "Molecular Basis of Neuronal Autophagy in Ageing: Insights from Caenorhabditis elegans." Cells 10, no. 3 (2021): 694. http://dx.doi.org/10.3390/cells10030694.

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Autophagy is an evolutionarily conserved degradation process maintaining cell homeostasis. Induction of autophagy is triggered as a response to a broad range of cellular stress conditions, such as nutrient deprivation, protein aggregation, organelle damage and pathogen invasion. Macroautophagy involves the sequestration of cytoplasmic contents in a double-membrane organelle referred to as the autophagosome with subsequent degradation of its contents upon delivery to lysosomes. Autophagy plays critical roles in development, maintenance and survival of distinct cell populations including neurons

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33

Sottile, Sarah Y., Lynne Ling, Brandon C. Cox, and Donald M. Caspary. "Impact of ageing on postsynaptic neuronal nicotinic neurotransmission in auditory thalamus." Journal of Physiology 595, no. 15 (2017): 5375–85. http://dx.doi.org/10.1113/jp274467.

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34

Mann, David M. A. "Neuronal loss in old people: The affects of ageing or disease?" Neurobiology of Aging 8, no. 6 (1987): 550–51. http://dx.doi.org/10.1016/0197-4580(87)90130-8.

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35

Dudek, Alicja, and Wojciech Zgliczyński. "Modern markers for the assessment of biological age." Wiedza Medyczna 5, no. 2 (2023): 1–9. http://dx.doi.org/10.36553/wm.156.

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The steady increase in human life expectancy in the 21st century is considered one of the major public health challenges. However, current achievements in longevity, are most often associated with increasing years in disability. Current studies indicate that healthy longevity is achieved, through harmonised ageing of the whole body. Due to the complexity of ageing, a number of biological age markers have been determined to describe the intensity of changes limiting biophysiological functions at different levels of the body. Biological age markers can be divided into two categories: parameters

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36

Ojo, Bunmi, Heather Davies, Payam Rezaie, et al. "Age-Induced Loss of Mossy Fibre Synapses on CA3 Thorns in the CA3 Stratum Lucidum." Neuroscience Journal 2013 (June 17, 2013): 1–8. http://dx.doi.org/10.1155/2013/839535.

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Advanced ageing is associated with hippocampal deterioration and mild cognitive decline. The hippocampal subregion CA3 stratum lucidum (CA3-SL) receives neuronal inputs from the giant mossy fibre boutons of the dentate gyrus, but relatively little is known about the integrity of this synaptic connection with ageing. Using serial electron microscopy and unbiased stereology, we examined age-related changes in mossy fibre synapses on CA3 thorny excrescences within the CA3-SL of young adults (4-month-old), middle-aged (12-month-old), and old-aged (28-month-old) Wistar rats. Our data show that whil

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37

Brazel, Christine Y., and Mahendra S. Rao. "Aging and neuronal replacement." Ageing Research Reviews 3, no. 4 (2004): 465–83. http://dx.doi.org/10.1016/j.arr.2004.04.003.

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38

Ritchie, Karen. "Establishing the limits of normal cerebral ageing and senile dementias." British Journal of Psychiatry 173, no. 2 (1998): 97–101. http://dx.doi.org/10.1192/bjp.173.2.97.

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Cognitive deterioration is so commonly observed in the elderly that it is considered by many to be an inevitable feature of the ageing process. Some researchers have proposed that the senile dementias are the inevitable end-point of this process, should the person live long enough. The differentiation of normal cerebral ageing from disease process is important in the selection of control groups for research, and also for clinical decision-making. In the latter context it is important to ask at what level of dysfunction intervention should occur, and whether this should be active or palliative.

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39

Rivera, Andrea D., Irene Chacon-De-La-Rocha, Francesca Pieropan, Maria Papanikolau, Kasum Azim, and Arthur M. Butt. "Keeping the ageing brain wired: a role for purine signalling in regulating cellular metabolism in oligodendrocyte progenitors." Pflügers Archiv - European Journal of Physiology 473, no. 5 (2021): 775–83. http://dx.doi.org/10.1007/s00424-021-02544-z.

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AbstractWhite matter (WM) is a highly prominent feature in the human cerebrum and is comprised of bundles of myelinated axons that form the connectome of the brain. Myelin is formed by oligodendrocytes and is essential for rapid neuronal electrical communication that underlies the massive computing power of the human brain. Oligodendrocytes are generated throughout life by oligodendrocyte precursor cells (OPCs), which are identified by expression of the chondroitin sulphate proteoglycan NG2 (Cspg4), and are often termed NG2-glia. Adult NG2+ OPCs are slowly proliferating cells that have the ste

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40

Scott, Brian, James Leu, and B. Cinader. "Effects of aging on neuronal electrical membrane properties." Mechanisms of Ageing and Development 44, no. 3 (1988): 203–14. http://dx.doi.org/10.1016/0047-6374(88)90022-x.

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41

Herrup, Karl. "ATM and the epigenetics of the neuronal genome." Mechanisms of Ageing and Development 134, no. 10 (2013): 434–39. http://dx.doi.org/10.1016/j.mad.2013.05.005.

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42

Disterhoft, John F., and M. Matthew Oh. "Alterations in intrinsic neuronal excitability during normal aging." Aging Cell 6, no. 3 (2007): 327–36. http://dx.doi.org/10.1111/j.1474-9726.2007.00297.x.

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43

Doms, Robert W. "Intracellular A-beta in neuronal and non-neuronal cells." Neurobiology of Aging 21 (May 2000): 70. http://dx.doi.org/10.1016/s0197-4580(00)82535-x.

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44

Lam, Philip Y., Fei Yin, Ryan T. Hamilton, Alberto Boveris, and Enrique Cadenas. "Elevated neuronal nitric oxide synthase expression during ageing and mitochondrial energy production." Free Radical Research 43, no. 5 (2009): 431–39. http://dx.doi.org/10.1080/10715760902849813.

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45

Toescu, Emil C., and Alexei Verkhratsky. "Neuronal ageing from an intraneuronal perspective: roles of endoplasmic reticulum and mitochondria." Cell Calcium 34, no. 4-5 (2003): 311–23. http://dx.doi.org/10.1016/s0143-4160(03)00142-8.

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46

Christina, Maria, W. De Avellar, and Regina P. Markus. "Neuronal uptake of noradrenaline in the rat isolated trachea: Effect of ageing." Comparative Biochemistry and Physiology Part C: Comparative Pharmacology 96, no. 2 (1990): 287–90. http://dx.doi.org/10.1016/0742-8413(90)90009-x.

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47

Capanni, Cristina, Stefano Squarzoni, Stefania Petrini, et al. "Increase of Neuronal Nitric Oxide Synthase in Rat Skeletal Muscle during Ageing." Biochemical and Biophysical Research Communications 245, no. 1 (1998): 216–19. http://dx.doi.org/10.1006/bbrc.1998.8404.

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48

Wu, Yue, Jinwei Pang, Jianhua Peng, et al. "Apolipoprotein E Deficiency Aggravates Neuronal Injury by Enhancing Neuroinflammation via the JNK/c-Jun Pathway in the Early Phase of Experimental Subarachnoid Hemorrhage in Mice." Oxidative Medicine and Cellular Longevity 2019 (December 26, 2019): 1–15. http://dx.doi.org/10.1155/2019/3832648.

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Neuronal injury is the primary cause of poor outcome after subarachnoid hemorrhage (SAH). The apolipoprotein E (APOE) gene has been suggested to be involved in the prognosis of SAH patients. However, the role of APOE in neuronal injury after SAH has not been well studied. In this study, SAH was induced in APOE-knockout (APOE-/-) and wild-type (WT) mice to investigate the impact of APOE deficiency on neuronal injury in the early phase of SAH. The experiments of this study were performed in murine SAH models in vivo and primary cultured microglia and neurons in vitro. The SAH model was induced b

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49

Wang, Lifen, Sonnet S. Davis, Martin Borch Jensen, et al. "JNK modifies neuronal metabolism to promote proteostasis and longevity." Aging Cell 18, no. 3 (2019): e12849. http://dx.doi.org/10.1111/acel.12849.

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50

Oh, Sangsoo, Hyun Seok Hong, Enmi Hwang, et al. "Amyloid peptide attenuates the proteasome activity in neuronal cells." Mechanisms of Ageing and Development 126, no. 12 (2005): 1292–99. http://dx.doi.org/10.1016/j.mad.2005.07.006.

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