Cited by 97Mitochondrial Function and PathologyNeuroscience and Neuropharmacology ResearchNeurological Disease Mechanisms and Treatments

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Axonal energy metabolism, and the effects in aging and neurodegenerative diseases

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Yang, Sen, Park, Jung Hyun, Lu, Hui-Chen·2023·Molecular Neurodegeneration

DOI 10.1186/s13024-023-00634-3PMC PMC10357692

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Abstract

Abstract Human studies consistently identify bioenergetic maladaptations in brains upon aging and neurodegenerative disorders of aging (NDAs), such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and Amyotrophic lateral sclerosis. Glucose is the major brain fuel and glucose hypometabolism has been observed in brain regions vulnerable to aging and NDAs. Many neurodegenerative susceptible regions are in the topological central hub of the brain connectome, linked by densely interconnected long-range axons. Axons, key components of the connectome, have high metabolic needs to support neurotransmission and other essential activities. Long-range axons are particularly vulnerable to injury, neurotoxin exposure, protein stress, lysosomal dysfunction, etc. Axonopathy is often an early sign of neurodegeneration. Recent studies ascribe axonal maintenance failures to local bioenergetic dysregulation. With this review, we aim to stimulate research in exploring metabolically oriented neuroprotection strategies to enhance or normalize bioenergetics in NDA models. Here we start by summarizing evidence from human patients and animal models to reveal the correlation between glucose hypometabolism and connectomic disintegration upon aging/NDAs. To encourage mechanistic investigations on how axonal bioenergetic dysregulation occurs during aging/NDAs, we first review the current literature on axonal bioenergetics in distinct axonal subdomains: axon initial segments, myelinated axonal segments, and axonal arbors harboring pre-synaptic boutons. In each subdomain, we focus on the organization, activity-dependent regulation of the bioenergetic system, and external glial support. Second, we review the mechanisms regulating axonal nicotinamide adenine dinucleotide (NAD + ) homeostasis, an essential molecule for energy metabolism processes, including NAD + biosynthetic, recycling, and consuming pathways. Third, we highlight the innate metabolic vulnerability of the brain connectome and discuss its perturbation during aging and NDAs. As axonal bioenergetic deficits are developing into NDAs, especially in asymptomatic phase, they are likely exaggerated further by impaired NAD + homeostasis, the high energetic cost of neural network hyperactivity, and glial pathology. Future research in interrogating the causal relationship between metabolic vulnerability, axonopathy, amyloid/tau pathology, and cognitive decline will provide fundamental knowledge for developing therapeutic interventions.

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Fig. 1 The spatial organization of glucose metabolism machineries across axon. A. Upper panel: Heat map description of the degree of energy consumption by each axonal activity within three axonal subdomains. Bottom panel: the intensity of each feature/parameter of glucose metabolism machineries within three axonal subdomains. Heat map color from white to dark represents the mild to strong degree/intensity. B.-D. The spatial organization of glucose transporters (GLUTs), monocarboxylic acid transporters (MCTs), glycolytic enzymes, mitochondria, and glial partners in axon initial segment (B), myelinated axonal shaft (C), and axonal arbors (D). D. The activity driven adaption of glucose metabolism machineries in presynaptic compartments. ① Activity dependent recruitment and anchoring of mitochondria to F actin filament at presynaptic sites through the AMPK-PAK-Syntaphilin axis; ② Neuronal stimulation induced mitochondrial ultrastructural changes with wider cristae and more compact or irregular matrices; ③ Surface mobilization of GLUT4, and presumably increased glucose uptake and glucose metabolism; and ④ Increased glucose metabolism through the Hexosamine synthesis pathway to boost O-GlcNAcylation of mitochondrial adaptor protein Milton, which reduce mitochondria mobilityCC BY · PubMed Central

Fig. 2 The molecular underpinnings of NAD redox potential maintenance in axons. A. A schematic view of NAD biosynthetic pathways. B. Heat map visualization of the abundance of mRNA and proteins of NAD biosynthetic enzymes. Transcript levels are adapted from [259]; protein levels are adapted from [260]. Abbreviations: Inh. Neu, inhibitory neurons; Exc. Neu, excitatory neurons; Mic. Mac., microglia and macrophages; Oligo, oligodendrocytes; OPC, oligodendrocyte precursor cells; Fibro.-like, fibroblast-like cells; End, endothelial cells. C. The subcellular localization of NMNAT1-3 in the soma and proximal axon. D. The subcellular distribution of NMNAT2, NMNAT3, and proteins involved in NAD+/NADH homeostasis in presynaptic boutons. (D1) NMNAT2, LDH-A, and glycolytic enzymes closely attach to synaptic vesicles; NMNAT2 inhibits SARM1 activation and maintains local NAD redox potential together with LDH-A to support “onboard” glycolysis; (D2) NMNAT3 inside mitochondrial matrix maintains local NAD redox potential together with OXPHO units, SLC25A51 (NAD+ transporter), and Malate-Aspartate shuttle. E. A hypothetical model of mitochondrial independent NAD+ recycling through the glutamine carboxylation pathway. MDH1, cytosolic malate dehydrogenase 1; ACLY, ATP citrate lyase; GLS, glutaminase; Gln, glutamine; Glu, glutamate; GOT1, glutamic-oxaloacetic transaminase 1; α-KG, alpha ketoglutarate; IDH1, isocitrate dehydrogenase (NADP+) 1; OAA, oxaloacetateCC BY · PubMed Central

Fig. 3 Aging induced bioenergetic maladaptation in mouse brain. A. Transcriptional fold change of enzymes involved in NAD+ redox potential maintenance in glutamatergic (GLUT), GABAergic (GABA), dopaminergic (DOPA) and cholinergic (CHOL) neurons upon aging, adapted from [22]. Sirt7 in aged cholinergic neurons is increased 5.97-fold, labeled in dark red. B. Transcriptional fold change of glycolytic enzymes and monocarboxylic acid transporters (MCTs) in myelin-forming oligodendrocytes (MF-OLG) and mature oligodendrocytes (MT-OLG). (MT-OLG-1 and MT-OLG-2 are two independent repeats in [22]). HK2 in aged myelin-forming oligodendrocytes is increased 9.72-fold, labeled in purple-red. C. A hypothetical model of the sequential events caused by aging that leads to metabolic failure in long-range axonal projections and glucose hypometabolism in central hubs of the brain connectomeCC BY · PubMed Central

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1 retracted

RETRACTED ARTICLE: Mapping NAD+ metabolism in the brain of ageing Wistar rats: potential targets for influencing brain senescence
Braidy, N., Poljak, A., Grant, R., Jayasena, T., Mansour, H., Chan‐Ling, T., Guillemin, G. J., Smythe, G. A., & Sachdev, P. S. (2013) · Biogerontology · doi:10.1007/s10522-013-9489-5 · Cited by 123
Retracted
Mapping the structural core of human cerebral cortex
Hagmann, P., Cammoun, L., Gigandet, X., Meuli, R., Honey, C. J., Wedeen, V. J., & Sporns, O. (2008) · PLoS Biology · doi:10.1371/journal.pbio.0060159 · Cited by 4,173 · cited 1×
“The majority of AD-susceptible regions identified are located in the default mode network (DMN), the topological central hub of the brain connectome [38, 39], containing densely interconnected long-range corticocortical axons [40, 41].”
Background
Clinical and biomarker changes in dominantly inherited Alzheimer's disease
Bateman, R. J., Xiong, C., Benzinger, T. L. S., Fagan, A. M., Goate, A., Fox, N. C., Marcus, D. S., Cairns, N. J., Xie, X., Blazey, T. M., et al. (2012) · New England Journal of Medicine · doi:10.1056/nejmoa1202753 · Cited by 3,814 · cited 1×
“Imaging: MRI, FDG‐PET, and PiB‐PET for 40 noncarriers and 88 PSEN1, PSEN2, APP mutation carriers Aimed to use data from longitudinal study to identify pathophysiological biomarkers • Mutation carriers 10–15 yrs before AD: Bilateral hippocampal atrophy, Precuneus glucose uptake↓ Episodic memory↓ [45]”
Method
Interplay between Cortical Spreading Depolarization and Seizures
Kramer, D. R., Fujii, T., Ohiorhenuan, I. E., & Liu, C. Y. (2017) · Stereotactic and Functional Neurosurgery · doi:10.1159/000452841 · Cited by 3,721
An Energy Budget for Signaling in the Grey Matter of the Brain
Attwell, D., & Laughlin, S. B. (2001) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1097/00004647-200110000-00001 · Cited by 3,543
Ageing as a risk factor for neurodegenerative disease
Hou, Y., Dan, X., Babbar, M., Wei, Y., Hasselbalch, S. G., Croteau, D. L., & Bohr, V. A. (2019) · Nature Reviews Neurology · doi:10.1038/s41582-019-0244-7 · Cited by 3,310 · cited 1×
“Aging is considered one of the biggest risk factors for dementia and sporadic late-onset neurodegenerative diseases [20].”
Background
Glutamate uptake into astrocytes stimulates aerobic glycolysis: a mechanism coupling neuronal activity to glucose utilization.
Pellerin, L., & Magistretti, P. J. (1994) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.91.22.10625 · Cited by 2,927 · cited 1×
“Because LDH-B favors the conversion in reverse direction to LDH-A, that is it consumes NAD+ and produces NADH and pyruvate [291, 292], LDH-B’s activity may counteract LDH-A, thus reducing NAD redox potential and restraining glycolysis.”
Background
The mechanism of eukaryotic translation initiation and principles of its regulation
Jackson, R. J., Hellen, C. U. T., & Pestova, T. V. (2010) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2838 · Cited by 2,759
Brain energy metabolism: focus on Astrocyte-neuron metabolic cooperation
Bélanger, M., Allaman, I., & Magistretti, P. J. (2011) · Cell Metabolism · doi:10.1016/j.cmet.2011.08.016 · Cited by 2,313
The role of the posterior cingulate cortex in cognition and disease
Leech, R., & Sharp, D. J. (2014) · Brain · doi:10.1093/brain/awt162 · Cited by 2,247

Show all 428 references

Research works printed but not linked: 2

Mc cluskey M. thesis: “Study of vesicular glycolysis in health and Huntington’s Disease” Université Grenoble Alpes [2020]. [GIN] Grenoble Institut des Neurosciences; 2021.
Magali V, Lena H, Jörn D, Ingvill T, Lars S, Marc N, Camila C-W, van den Barbara H, Øyvind S, Roland S, et al. Chronic depletion of subcellular NAD pools reveals their interconnectivity and a buffering function of mitochondria. Nature Portfolio; 2022.

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Risco-Acevedo, D., Subirós, N., Camacho, H., Ramírez-Sánchez, J., Rodríguez-Virulich, Y., Etchegoyen-Amoros, A., Fuentes-Morales, D., Palenzuela, D. O., Pérez-Saad, H., & García-del-Barco-Herrera, D. (2025) · Experimental Brain Research · doi:10.1007/s00221-025-07183-9 · Cited by 3
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Xu, H., Wang, G., Jiang, Z., Han, Y., Zhao, W., Zhang, H., Liu, H., Liu, H., Li, Z., & Ji, F. (2025) · Advanced Healthcare Materials · doi:10.1002/adhm.202500941 · Cited by 3
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Özalay, Ö., Mediavilla, T., Giacobbo, B. L., Marcellino, D. J., Orädd, G., Rieckmann, A., & Sultan, F. R. (2025) · Brain Structure and Function · doi:10.1007/s00429-025-03040-1 · Cited by 2
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Chang, Y. C., Yang, S., Cho, M., Nho, K. T., Baizabal, J., & Lu, H. (2025) · FEBS Journal · doi:10.1111/febs.70322 · Cited by 4
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Functionalized nanozyme delivery of a KCC2-activator conjugate for the promotion of functional recovery after acute spinal cord injury
Zhao, H., Lin, S., Chen, H., Yang, L., Gao, K., & Mei, X. (2025) · Materials Today Bio · doi:10.1016/j.mtbio.2025.102624 · Cited by 2
“Among various metabolic pathways, aerobic glucose metabolism is especially critical for neurons, supporting their high energy demand and diverse physiological activities [2].”
Aging-Related Changes in the Injury Response of the Peripheral Nervous System
Cen, Y.-Y., Wang, M.-Y., Song, Q., Gao, X.-L., Zhou, C., Li, C.-J., Liu, F., Zhang, Y.-Y., & Shen, J. (2026) · Neuroscience Bulletin · doi:10.1007/s12264-025-01564-4 · Cited by 2
“However, the age-related impairments in oxidative phosphorylation (OXPHOS), reduced NAD+ levels, and a disrupted TCA cycle collectively cripple ATP production and deprive the cell of essential biosynthetic precursors[247, 277–279].”
Effects of Time-Dependent Adenosine Triphosphate Consumption Caused by Neuron Firing on Adenosine Triphosphate Concentrations in Synaptic Boutons Containing and Lacking a Stationary Mitochondrion
Kuznetsov, A. V. (2024) · Journal of Biomechanical Engineering · doi:10.1115/1.4065743 · Cited by 2
Modeling of ATP transport in an axon: Effects of spontaneous neuron firing and mitochondrial transfer via tunneling nanotubes
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Drumond‐Bock, A. L., & Beckstead, M. J. (2025) · European Journal of Neuroscience · doi:10.1111/ejn.70025 · Cited by 1
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Drumond‐Bock, A. L., Blankenship, H. E., Pham, K. D., Carter, K. A., Freeman, W. M., & Beckstead, M. J. (2025) · eNeuro · doi:10.1523/eneuro.0107-25.2025 · Cited by 3
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Zhang, L., Cai, L., Lin, H., Wu, W., Zhu, L., Cai, J., Hu, C., Lin, X., Sun, H., & Wei, X. (2025) · European Journal of Neuroscience · doi:10.1111/ejn.70221 · Cited by 1
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Zhang, H., Ya, J., Liao, X., Du, X., Zhao, C., Ren, J., & Qu, X. (2025) · Small · doi:10.1002/smll.202509547 · Cited by 1
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SARAK, E. B. G. Ö. G., & Ceylan, Y. (2025) · Bartın University International Journal of Natural and Applied Sciences · doi:10.55930/jonas.1741124 · Cited by 1
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Miao, K., Meng, M., Liu, L., Li, M., Bai, Y., Guo, Y., Zhang, G., Kong, J., & Mu, J. (2026) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-026-01729-3 · Cited by 1
“Indeed, most of this ATP is consumed by Na⁺/K⁺-ATPase to restore ionic gradients (Yang et al. 2023; Shrivastava et al. 2020 ).”
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Jia, Q., Li, Z., Yang, T., Yang, W., & Chi, W. (2026) · Immunity Inflammation and Disease · doi:10.1002/iid3.70469 · Cited by 1
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Qian, J., Wang, H., Zhang, Y., Cui, J., Cao, Y., Xie, J., & Shi, L. (2026) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2026.106840 · Cited by 1
Early disruptions in brain capillary blood flow control in a mouse model of Alzheimer’s disease
Hariharan, A., Vigderman, A. S., Isaacs, D. P., Weir, N., Park, G., Edwards, S., & Longden, T. A. (2026) · The Journal of General Physiology · doi:10.1085/jgp.202614014 · Cited by 1
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Application of proteomics in brain's aging research
Tan, Y., Luo, F., Wei, Y., & Liu, P. (2024) · Human Brain · doi:10.37819/hb.3.1778
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Park, J. H., Kim, B., Al‐Amin, M. M., Tate, M. D., Sharify, A. D., John, S. K., Karahan, H., Lu, H., Dabin, L. C., & Kim, J. (2026) · Alzheimer's & Dementia · doi:10.1002/alz.71742
“65,66 Furthermore, CellChat analysis inferred significantly increased communication among the O_3 and M_2 clusters, with additional involvement of the M_1 cluster, in immune-relevant pathways such as PROS and VISTA (Figures 5D and S5C).”
Self-citation
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Shao, W., Liu, X., Chen, L., Xuedong, Z., Wu, Q., Bu, C., Zheng, F., Yu, G., Hu, H., Guo, Z., et al. (2025) · SSRN Electronic Journal · doi:10.2139/ssrn.5147375
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Absolute quantification of brain deuterium metabolic imaging in healthy volunteers and glioblastoma patients at 7TPreprint
Karkouri, J., Novoselova, M., Miller, S., Zhang, M., Constantinou, A., Graf, C., Atkinson, D., Tramm, B., Schillak, S., Mair, R. J., et al. (2025) · medRxiv · doi:10.1101/2025.10.08.25337571
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Yin, C., Kindt, A. S. D., Harms, A. C., Hartman, R., Hankemeier, T., & de Lange, E. C. M. (2025) · Metabolomics · doi:10.1007/s11306-025-02350-z
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Additional file 1 of Pathological characteristics of axons and alterations of proteomic and lipidomic profiles in midbrain dopaminergic neurodegeneration induced by WDR45-deficiency
Wang, P., Shao, Y., Al-Nusaif, M., Zhang, J., Yang, H., Yang, Y., Kim, K., Li, S., Liu, C., Cai, H., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26943114
Additional file 2 of Pathological characteristics of axons and alterations of proteomic and lipidomic profiles in midbrain dopaminergic neurodegeneration induced by WDR45-deficiency
Wang, P., Shao, Y., Al-Nusaif, M., Zhang, J., Yang, H., Yang, Y., Kim, K., Li, S., Liu, C., Cai, H., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26943117
Additional file 3 of Pathological characteristics of axons and alterations of proteomic and lipidomic profiles in midbrain dopaminergic neurodegeneration induced by WDR45-deficiency
Wang, P., Shao, Y., Al-Nusaif, M., Zhang, J., Yang, H., Yang, Y., Kim, K., Li, S., Liu, C., Cai, H., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26943120
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Zhou, H., Xu, G., Chen, Q., Liu, Y., Li, S., Huo, N., Liu, J., Wang, W., Yang, N., & Zhou, N. (2026) · Experimental Neurology · doi:10.1016/j.expneurol.2026.115715
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Dai, X., Zhang, Z., Ge, X., Zhou, H., Yu, P., Li, Y., Chen, S., Huang, J.-L., Wu, Q., & Liang, J. (2026) · Research Square · doi:10.21203/rs.3.rs-9024544/v1
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Ye, H.-L., Zheng, X.-X., Li, M.-M., Zhang, Z.-Q., Chen, L.-X., Zhang, W.-J., Fan, R. C.-H., He, G., & Xu, A.-C. (2026) · Chemico-Biological Interactions · doi:10.1016/j.cbi.2026.112118
Age-related changes to brain energetics revealed by PET/MRI imaging
Bevington, C. W. J., Dhaliwal, S., McKenzie, J., Stoessl, A. J., & Sossi, V. (2026) · NeuroImage Clinical · doi:10.1016/j.nicl.2026.104014
Nicotinamide nucleotide transhydrogenase deficiency impairs neuronal function via energy metabolism dysregulation in Alzheimer's disease
Wan, X., Lu, W., Liu, S., Zhao, Y., Hu, J., Ding, X., Gu, P., Zou, Y., Jiang, B., & Yang, Y. (2026) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2026.05.341
Evaluation of retinal nerve fiber layer and choroidal thickness in patients with methamphetamine use disorder
Muhammad, H., Yasin, M. A. B. M., Jaafar, J., Hou, L. J., & Hitam, W. H. W. (2026) · Taiwan Journal of Ophthalmology · doi:10.4103/tjo.tjo-d-25-00165
Volume electron microscopy in axon regeneration research: insights into mitochondria, endoplasmic reticulum, and membrane contacts
Tamada, H. (2026) · Frontiers in Neural Circuits · doi:10.3389/fncir.2026.1870424
“Although the mechanisms responsible for mitochondrial exclusion from the healthy AIS remain unclear (Yang et al., 2023), the accumulation of mitochondria under pathological conditions may reflect a protective cellular response.”
Synaptic dysfunction as a major driver in Alzheimer's disease: Beyond the amyloid paradigm
Mierzwa, N., & Wężyk, M. (2026) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2026.106858
A systematic review and meta-analysis of OCT-based ophthalmic changes in amyotrophic lateral sclerosis
Ahsan, A., Ou, J., Majumder, P., Chiang, Y. H., Huang, J. K., & Huang, C.-C. S. (2026) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2026.579028
Neurons Die Not by One Hit, but by Signaling Convergence
Chauhan, D., Goel, F., & Rajput, M. S. (2026) · Molecular Neurobiology · doi:10.1007/s12035-026-06093-3
Mitochondrial Dysfunction as a Driver of Meta-Inflammation in Aging: The Emerging Role of PDK4 in Bioenergetic Reprogramming and Inflammatory Amplification
Chowdhury, M. R., Jeong, G.-H., & Lee, I. (2026) · Cells · doi:10.3390/cells15151404
“Mitochondrial impairment in neurons can reduce ATP availability, increase mtROS, disturb calcium buffering, and weaken synaptic resilience [49].”
Neuronal Prps is required for synaptic development and locomotor function in Drosophila melanogaster
Dang, T. N., & Yoshida, H. (2026) · Gene · doi:10.1016/j.gene.2026.150361 · Cited by 1
Extracellular vesicles carrying the tenascin-C protein participate in glucose metabolism in neurodegenerative injury via inhibiting the AKT/GLUT1 pathway
Liu, X., Chen, L., Zhu, X., Wu, Q., Bu, C., Zheng, F., Yu, G., Hu, H., Guo, Z., Zhou, J., et al. (2026) · Chemico-Biological Interactions · doi:10.1016/j.cbi.2026.112318
Repurposing Antidiabetic Drugs in Neurodegenerative Disorders: From Preclinical Mechanisms to Clinical Evidence
Devi, D., Rani, A., Singh, J., Quasmi, M. N., Jangra, A., & Kumar, D. (2026) · SN Comprehensive Clinical Medicine · doi:10.1007/s42399-026-02731-y
“Additionally, vascular diseases impact the cognitive functions and contribute to cognitive decline due to decreased cerebral blood flow, which affects the metabolism of glucose [ 12].”
Bone regulates locomotion by sustaining motoneuronal mitochondrial functionPreprint
Romeo-Guitart, D., Tirani, T., Milunov, D., Torres-Juacida, A. K., Lamotte, B., Arenas-Plascencia, C., Durand, S., Nemazanyy, I., Moriceau, S., Saha, S., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.10.07.750453
Macroscopic cerebral energy efficiency corresponds to neuron reorganization in awake and anesthetized mice
Wang, D., Li, H., Zeng, Y., Gao, J., Xu, M., Bo, B., Pei, M., Liang, Z., Zhou, N., & Thompson, G. J. (2026) · Frontiers in Neuroscience · doi:10.3389/fnins.2026.1949911
“In Alzheimer’s disease models, neuronal injury in affected cortical regions leads to astrocyte damage (Verkhratsky et al., 2017; Toledano-Diaz et al., 2022), contributing to vascular dysfunction and reduced CBF (Amtul et al., 2020), ultimately impacting CMR O2 (Yang et al., 2023).”
Nutrients and Their Role in Autophagy Regulation
Wilson, N., Koçak, G., Sarkar, S., Ruiz, Y. R., & Korolchuk, V. I. (2026) · Biochemistry · doi:10.1021/acs.biochem.6c00482

Authors: Yang, S., Park, J. H., & Lu, H.-C.
Affiliations: Indiana University Bloomington (US)
Corresponding author: Lu, Hui-Chen
ORCID: Yang, Sen
Lu, Hui-Chen
Venue: Molecular Neurodegeneration
Publisher: Springer Science and Business Media LLC
Published: 2023-07-20
Volume: 18
Issue: 1
Pages: 49-49
ISSN: 1750-1326 (ISSN-L)
DOI: 10.1186/s13024-023-00634-3
PMC: PMC10357692
OpenAlex: W4384925673
Cited by: 94
References: 428
Citations by year: 2026: 25 · 2025: 37 · 2024: 28 · 2023: 4
FWCI: 2.54
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
creativecommons.org/licenses/by/4.0 (tdm)
creativecommons.org/licenses/by/4.0 (vor)
Locations: Molecular Neurodegeneration (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders: NINDS (NS086794)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords: axonal energy metabolism, axonopathy, neurodegenerative diseases, brain aging, glucose hypometabolism, brain connectome, long-range axons, axon initial segment, myelinated axons, axonal arbors, NAD+ homeostasis, NAD biosynthesis, NAD+ recycling, neuroprotection, Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, cognitive decline
MeSH terms: Aging, Animals, Axons, Energy Metabolism, Glucose, Humans, NAD, Neurodegenerative Diseases

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Axonal energy metabolism, and the effects in aging and neurodegenerative diseases

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