The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.
Ageing and neuronal vulnerability
Abstract
Everyone ages, but only some will develop a neurodegenerative disorder in the process. Disease might occur when cells fail to respond adaptively to age-related increases in oxidative, metabolic and ionic stress, thereby resulting in the accumulation of damaged proteins, DNA and membranes. Determinants of neuronal vulnerability might include cell size and location, metabolism of disease-specific proteins and a repertoire of signal transduction pathways and stress resistance mechanisms. Emerging evidence on protein interaction networks that monitor and respond to the normal ageing process suggests that successful neural ageing is possible for most people, but also cautions that cures for neurodegenerative disorders are unlikely in the near future.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Neuroinflammation can directly damage neurons, impair synaptic plasticity, and disrupt neuronal networks, leading to cognitive decline and functional impairments.
“Neuroinflammation can directly damage neurons, impair synaptic plasticity, and disrupt neuronal networks, leading to cognitive decline and functional impairments5–7.”
From MT1-MMP inhibition rejuvenates ageing brain and rescues cognitive deficits in obesity (2025) · cites this paper as [6]
Citations
Cites
Amyloid oligomers exacerbate tau pathology in a mouse model of tauopathy
Selenica, M.-L. B., Brownlow, M., Jimenez, J. P., Lee, D. C., Pena, G., Dickey, C. A., Gordon, M. N., & Morgan, D. (2013) · Neurodegenerative Diseases · doi:10.1159/000337230 · Cited by 10,359
Triple-Transgenic Model of Alzheimer’s Disease with Plaques and Tangles
Oddo, S., Caccamo, A., Shepherd, J. D., Murphy, M. P., Golde, T. E., Kayed, R., Metherate, R., Mattson, M. P., Akbari, Y., & LaFerla, F. M. (2003) · Neuron · doi:10.1016/s0896-6273(03)00434-3 · Cited by 4,126
Self-citationAssociation of missense and 5′-splice-site mutations in tau with the inherited dementia FTDP-17
Hutton, M., Lendon, C. L., Rizzu, P., Baker, M., Froelich, S., Houlden, H., Pickering-Brown, S., Chakraverty, S., Isaacs, A., Grover, A., et al. (1998) · Nature · doi:10.1038/31508 · Cited by 3,498
Immunization with amyloid-β attenuates Alzheimer-disease-like pathology in the PDAPP mouse
Schenk, D., Barbour, R., Dunn, W., Gordon, G., Grajeda, H., Guido, T., Hu, K., Huang, J., Johnson-Wood, K., Khan, K., et al. (1999) · Nature · doi:10.1038/22124 · Cited by 3,160
Impaired Degradation of Mutant α-Synuclein by Chaperone-Mediated Autophagy
Cuervo, A. M., Stefanis, L., Fredenburg, R., Lansbury, P. T., & Sulzer, D. (2004) · Science · doi:10.1126/science.1101738 · Cited by 2,024 · cited 1×
“Such protein aggregates might arise, in part, as a consequence of impaired proteasomal and/or autophagic removal of the (oxidatively) damaged protein”
BackgroundGene regulation and DNA damage in the ageing human brain
Lu, T., Pan, Y., Kao, S.-Y., Li, C., Kohane, I., Chan, J., & Yankner, B. A. (2004) · Nature · doi:10.1038/nature02661 · Cited by 1,874
Apoptosis in neurodegenerative disorders
Mattson, M. P. (2000) · Nature Reviews Molecular Cell Biology · doi:10.1038/35040009 · Cited by 1,605
Self-citationABAD Directly Links Aß to Mitochondrial Toxicity in Alzheimer's Disease
Lustbader, J. W., Cirilli, M., Lin, C., Xu, H. W., Takuma, K., Wang, N., Caspersen, C., Chen, X., Pollak, S., Chaney, M., et al. (2004) · Science · doi:10.1126/science.1091230 · Cited by 1,303
The changing landscape of ischaemic brain injury mechanisms
Lee, J.-M., Zipfel, G. J., & Choi, D. W. (1999) · Nature · doi:10.1038/399a007 · Cited by 1,102
Early mitochondrial calcium defects in Huntington's disease are a direct effect of polyglutamines
Panov, A. V., Gutekunst, C.-A., Leavitt, B. R., Hayden, M. R., Burke, J. R., Strittmatter, W. J., & Greenamyre, J. T. (2002) · Nature Neuroscience · doi:10.1038/nn884 · Cited by 1,030
Immunoglobulins and complement factors in senile plaques: An immunoperoxidase study
Eikelenboom, P., & Stam, F. C. (1982) · Acta Neuropathologica · doi:10.1007/bf00685397 · Cited by 454
Duan, W., Guo, Z., Jiang, H., Ware, M., Li, X.-J., & Mattson, M. P. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0536856100 · Cited by 428
Self-citationItagaki, S., McGeer, P. L., & Akiyama, H. (1988) · Neuroscience Letters · doi:10.1016/0304-3940(88)90690-8 · Cited by 271
Keller, J. (2002) · Ageing Research Reviews · doi:10.1016/s1568-1637(01)00006-x · Cited by 247
Flagged first, then by citations
Research works printed but not linked: 212
- Hofer, S. M., Berg, S. & Era, P. Evaluating the interdependence of aging-related changes in visual and auditory acuity, balance, and cognitive functioning. Psychol. Aging 18, 285–305 (2003). · DOI
- Mattson, M. P. Pathways towards and away from Alzheimer's disease. Nature 430, 631–639 (2004). This review integrates information on the molecular pathogenesis of AD and efforts to prevent and treat this disorder. · DOI · Paper page
- Cookson, M. R. The biochemistry of Parkinson's disease. Annu. Rev. Biochem. 74, 29–52 (2005). · DOI
- Moore, D. J., West, A. B., Dawson, V. L. & Dawson, T. M. Molecular pathophysiology of Parkinson's disease. Annu. Rev. Neurosci. 27, 57–87 (2005). Reviews the involvement of mitochondrial dysfunction and perturbed ubiquitin-mediated proteolysis in PD. · DOI
- Sieradzan, K. A. & Mann, D. M. The selective vulnerability of nerve cells in Huntington's disease. Neuropathol. Appl. Neurobiol. 27, 1–21 (2001). · DOI
- Cleveland, D. W. & Rothstein, J. D. From Charcot to Lou Gehrig: deciphering selective motor neuron death in ALS. Nature Rev. Neurosci. 2, 806–819 (2001). · DOI
- Serrano, F. & Klann, E. Reactive oxygen species and synaptic plasticity in the aging hippocampus. Ageing Res. Rev. 3, 431–443 (2004). · DOI
- Zecca, L., Youdim, M. B., Riederer, P., Connor, J. R. & Crichton, R. R. Iron, brain ageing and neurodegenerative disorders. Nature Rev. Neurosci. 5, 863–873 (2004). · DOI · Paper page
- Ames, B. N. Delaying the mitochondrial decay of aging. Ann. NY Acad. Sci. 1019, 406–411 (2004). · DOI
- Gray, D. A., Tsirigotis, M. & Woulfe, J. Ubiquitin, proteasomes, and the aging brain. Sci. Aging Knowledge Environ. RE6 27 Aug 2003. · DOI
- Trojanowski, J. Q. & Mattson, M. P. Overview of protein aggregation in single, double, and triple neurodegenerative brain amyloidoses. Neuromolecular Med. 4, 1–6 (2003). · DOI
- Kyng, K. J. & Bohr, V. A. Gene expression and DNA repair in progeroid syndromes and human aging. Ageing Res. Rev. 4, 579–602 (2005). · DOI · Paper page
- Butler, R. N. et al. Longevity genes: from primitive organisms to humans. J. Gerontol. A Biol. Sci. Med. Sci. 58, 581–584 (2003). · DOI
- Wolkow, C. A. Life span: getting the signal from the nervous system. Trends Neurosci. 25, 212–216 (2002). Describes how insulin-like signalling in the nervous system might regulate ageing and determine lifespan. · DOI
- Mattson, M. P. Methylation and acetylation in nervous system development and neurodegenerative disorders. Ageing Res. Rev. 2, 329–342 (2003). · DOI
- Yehuda, S., Rabinovitz, S., Carasso, R. L. & Mostofsky, D. I. The role of polyunsaturated fatty acids in restoring the aging neuronal membrane. Neurobiol. Aging 23, 843–853 (2002). · DOI
- Floyd, R. A. & Hensley, K. Oxidative stress in brain aging. Implications for therapeutics of neurodegenerative diseases. Neurobiol. Aging 23, 795–807 (2002). · DOI
- Jenner, P. Oxidative stress in Parkinson's disease. Ann. Neurol. 53, S26–S36 (2003). · DOI · Paper page
- Pedersen, W. A. et al. Protein modification by the lipid peroxidation product 4-hydroxynonenal in the spinal cords of amyotrophic lateral sclerosis patients. Ann. Neurol. 44, 819–824 (1998). · DOI
- Rakhit, R. et al. Monomeric Cu,Zn-superoxide dismutase is a common misfolding intermediate in the oxidation models of sporadic and familial amyotrophic lateral sclerosis. J. Biol. Chem. 279, 15499–15504 (2004). · DOI
- Grondin, R. et al. Chronic, controlled GDNF infusion promotes structural and functional recovery in advanced parkinsonian monkeys. Brain 125, 2191–2201 (2002). · DOI
- Zuccato, C. et al. Huntingtin interacts with REST/NRSF to modulate the transcription of NRSE-controlled neuronal genes. Nature Genet. 35, 76–83 (2003). · DOI · Paper page
- Weindruch, R. & Sohal, R. S. Seminars in medicine of the Beth Israel Deaconess Medical Center. Caloric intake and aging. N. Engl. J. Med. 337, 986–994 (1997). · DOI
- Heilbronn, L. K. & Ravussin, E. Calorie restriction and aging: review of the literature and implications for studies in humans. Am. J. Clin. Nutr. 78, 361–369 (2003). · DOI · Paper page
- Mattison, J. A., Lane, M. A., Roth, G. S. & Ingram, D. K. Calorie restriction in rhesus monkeys. Exp. Gerontol. 38, 35–46 (2003). · DOI
- Fontana, L., Meyer, T. E., Klein, S. & Holloszy, J. O. Long-term calorie restriction is highly effective in reducing the risk for atherosclerosis in humans. Proc. Natl Acad. Sci. USA 101, 6659–6663 (2004). · DOI · Paper page
- Mattson, M. P. Energy intake, meal frequency, and health: a neurobiological perspective. Annu. Rev. Nutr. 25, 237–260 (2005). · DOI
- Patel, N. V. et al. Caloric restriction attenuates Aβ-deposition in Alzheimer transgenic models. Neurobiol. Aging 26, 995–1000 (2005). · DOI · Paper page
- Maswood, N. et al. Caloric restriction increases neurotrophic factor levels and attenuates neurochemical and behavioral deficits in a primate model of Parkinson's disease. Proc. Natl Acad. Sci. USA 101, 18171–18176 (2004). · DOI
- Yu, Z. F. & Mattson, M. P. Dietary restriction and 2-deoxyglucose administration reduce focal ischemic brain damage and improve behavioral outcome: evidence for a preconditioning mechanism. J. Neurosci. Res. 57, 830–839 (1999). · DOI
- Mattson, M. P., Maudsley, S. & Martin, B. BDNF and 5-HT: a dynamic duo in age-related neuronal plasticity and neurodegenerative disorders. Trends Neurosci. 27, 589–594 (2004). · DOI · Paper page
- Barja, G. Free radicals and aging. Trends Neurosci. 27, 595–600 (2004). · DOI · Paper page
- Cotman, C. W. & Berchtold, N. C. Exercise: a behavioral intervention to enhance brain health and plasticity. Trends Neurosci. 25, 295–301 (2002). · DOI · Paper page
- Spires, T. L. Environmental enrichment rescues protein deficits in a mouse model of Huntington's disease, indicating a possible disease mechanism. J. Neurosci. 24, 2270–2276 (2004). · DOI
- Liu, D. et al. Mitochondrial UCP4 induces a glycolytic shift in energy metabolism and increases the resistance of neurons to oxidative stress. Neuromolecular Med. (in the press).
- Parker, J. A. et al. Resveratrol rescues mutant polyglutamine cytotoxicity in nematode and mammalian neurons. Nature Genet. 37, 349–350 (2005). · DOI
- Morrison, B. M., Hof, P. R. & Morrison, J. H. Determinants of neuronal vulnerability in neurodegenerative diseases. Ann. Neurol. 44, S32–S44 (1998). · DOI
- Smith, D. E., Saji, M., Joh, T. H., Reis, D. J. & Pickel, V. M. Ibotenic acid-induced lesions of striatal target and projection neurons: ultrastructural manifestations in dopaminergic and non-dopaminergic neurons and in glia. Histol. Histopathol. 2, 251–263 (1987).
- Mandelkow, E. M., Stamer, K., Vogel, R., Thies, E. & Mandelkow, E. Clogging of axons by tau, inhibition of axonal traffic and starvation of synapses. Neurobiol. Aging 24, 1079–1085 (2003). · DOI
- Bayatti, N. & Behl, C. The neuroprotective actions of corticotropin releasing hormone. Ageing Res. Rev. 4, 258–270 (2005). · DOI
- Ishunina, T. A. & Swaab, D. F. Neurohypophyseal peptides in aging and Alzheimer's disease. Ageing Res. Rev. 1, 537–558 (2002). · DOI
- Braak, H. & Braak, E. Evolution of neuronal changes in the course of Alzheimer's disease. J. Neural Transm. Suppl. 53, 127–140 (1998). · DOI
- Braak, H. et al. Staging of brain pathology related to sporadic Parkinson's disease. Neurobiol. Aging 24, 197–211 (2003). · DOI · Paper page
- Mills, K. R. The natural history of central motor abnormalities in amyotrophic lateral sclerosis. Brain 126, 2558–2566 (2003). · DOI
- Yuan, J. & Yankner, B. A. Apoptosis in the nervous system. Nature 407, 802–809 (2000). Reviews evidence that supports a role for apoptosis in the pathogenesis of neurodegenerative disorders. · DOI
- Miller, F. D., Pozniak, C. D. & Walsh, G. S. Neuronal life and death: an essential role for the p53 family. Cell Death Differ. 7, 880–888 (2000). · DOI
- Tanaka, Y. et al. Inducible expression of mutant α-synuclein decreases proteasome activity and increases sensitivity to mitochondria-dependent apoptosis. Hum. Mol. Genet. 10, 919–926 (2001). · DOI
- Akhtar, R. S., Ness, J. M. & Roth, K. A. Bcl-2 family regulation of neuronal development and neurodegeneration. Biochim. Biophys. Acta 1644, 189–203 (2004). · DOI
- Cheung, E. C. et al. Apoptosis-inducing factor is a key factor in neuronal cell death propagated by BAX-dependent and BAX-independent mechanisms. J. Neurosci. 25, 1324–1334 (2005). · DOI
- Wang, K. K. Calpain and caspase: can you tell the difference? Trends Neurosci. 23, 20–26 (2000). · DOI
- Stefanis, L. Caspase-dependent and -independent neuronal death: two distinct pathways to neuronal injury. Neuroscientist 11, 50–62 (2005). · DOI
- Chan, S. L. et al. Presenilin-1 mutations sensitize neurons to DNA damage-induced death by a mechanism involving perturbed calcium homeostasis and activation of calpains and caspase-12. Neurobiol. Dis. 11, 2–19 (2002). · DOI
- Brown, D. & Tatton, N. Apoptosis in Parkinson's disease: signals for neuronal degradation. Ann. Neurol. 53 (Suppl. 3), S61–S70 (2003).
- Crocker, S. J. et al. Inhibition of calpains prevents neuronal and behavioral deficits in an MPTP mouse model of Parkinson's disease. J. Neurosci. 23, 4081–4091 (2003). · DOI
- Gafni, J. & Ellerby, L. M. Calpain activation in Huntington's disease. J. Neurosci. 22, 4842–4849 (2002). · DOI
- Friedlander, R. M. Apoptosis and caspases in neurodegenerative diseases. N. Engl. J. Med. 348, 1365–1375 (2003). · DOI
- Mattson, M. P. & Kroemer, G. Mitochondria in cell death: novel targets for neuroprotection and cardioprotection. Trends Mol. Med. 9, 196–205 (2003). · DOI
- Glazner, G. W. et al. Endoplasmic reticulum D-myo-inositol 1,4,5-trisphosphate-sensitive stores regulate nuclear factor-κB binding activity in a calcium-independent manner. J. Biol. Chem. 276, 22461–22467 (2001). · DOI
- Milhavet, O. et al. Involvement of Gadd153 in the pathogenic action of presenilin-1 mutations. J. Neurochem. 83, 673–681 (2002). · DOI
- Boehning, D. et al. Cytochrome c binds to inositol (1,4,5) trisphosphate receptors, amplifying calcium-dependent apoptosis. Nature Cell Biol. 5, 1051–1061 (2003). · DOI
- Culmsee, C. & Mattson, M. P. p53 in neuronal apoptosis. Biochem. Biophys. Res. Commun. 331, 761–777 (2005). · DOI
- Kruman, I. et al. Evidence that 4-hydroxynonenal mediates oxidative stress-induced neuronal apoptosis. J. Neurosci. 17, 5089–5100 (1997). · DOI
- Bruckner, S. R., Perry, G. & Estus, S. 4-hydroxynonenal contributes to NGF withdrawal-induced neuronal apoptosis. J. Neurochem. 85, 999–1005 (2003). · DOI
- Zhou, H., Li, X. M., Meinkoth, J. & Pittman, R. N. Akt regulates cell survival and apoptosis at a postmitochondrial level. J. Cell Biol. 151, 483–494 (2000). · DOI
- Cutler, R. G. et al. Involvement of oxidative stress-induced abnormalities in ceramide and cholesterol metabolism in brain aging and Alzheimer's disease. Proc. Natl Acad. Sci. USA 101, 2070–2075 (2004). Links age-related alterations in the metabolism of membrane lipids to oxidative stress and neuronal degeneration in AD. · DOI · Paper page
- Haughey, N. J. et al. Perturbation of sphingolipid metabolism and ceramide production in HIV-dementia. Ann. Neurol. 55, 257–267 (2004). · DOI
- Cutler, R. G. et al. Evidence that accumulation of ceramides and cholesterol esters mediates oxidative stress-induced death of motor neurons in amyotrophic lateral sclerosis. Ann. Neurol. 52, 448–457 (2002). · DOI
- White, L. D. & Barone, S. Jr Qualitative and quantitative estimates of apoptosis from birth to senescence in the rat brain. Cell Death Differ. 8, 345–356 (2001). · DOI
- Hiona, A. & Leeuwenburgh, C. Life-long caloric restriction counteracts apoptotic effects of aging in the brain and bolsters the action of apoptosis inhibitors. Neurobiol. Aging. 26 Sep 2006 (doi: 10.1016/j.neurobiolaging.2005.08.006). · DOI
- Kempermann, G., Kuhn, H. G. & Gage, F. H. Experience-induced neurogenesis in the senescent dentate gyrus. J. Neurosci. 18, 3206–3212 (1998). Evidence that age-related declines in hippocampal neurogenesis can be counteracted by cognitive stimulation. · DOI · Paper page
- Sun, W. et al. Programmed cell death of adult-generated hippocampal neurons is mediated by the proapoptotic gene Bax. J. Neurosci. 24, 11205–11213 (2004). · DOI
- Haughey, N. J. et al. Disruption of neurogenesis by amyloid β-peptide, and perturbed neural progenitor cell homeostasis, in models of Alzheimer's disease. J. Neurochem. 83, 1509–1524 (2002). · DOI · Paper page
- Jin, K. et al. Increased hippocampal neurogenesis in Alzheimer's disease. Proc. Natl Acad. Sci. USA 101, 343–347 (2004). · DOI · Paper page
- Mattson, M. P. Excitotoxic and excitoprotective mechanisms: abundant targets for the prevention and treatment of neurodegenerative disorders. Neuromolecular Med. 3, 65–94 (2003). · DOI
- Ben-Ari, Y. & Cossart, R. Kainate, a double agent that generates seizures: two decades of progress. Trends Neurosci. 23, 580–587 (2000). · DOI
- Perl, T. M. et al. An outbreak of toxic encephalopathy caused by eating mussels contaminated with domoic acid. N. Engl. J. Med. 323, 1631–1633 (1990). · DOI
- Kisby, G. E., Ellison, M. & Spencer, P. S. Content of the neurotoxins cycasin (methylazoxymethanol β-D-glucoside) and BMAA (β-N-methylamino-L-alanine) in cycad flour prepared by Guam Chamorros. Neurology 42, 1336–1340 (1992). · DOI
- Langston, J. W., Ballard, P., Tetrud, J. W. & Irwin, I. Chronic parkinsonism in humans due to a product of meperidine-analog synthesis. Science 219, 979–980 (1983). First direct evidence that an environmental neurotoxin can cause parkinsonism. · DOI · Paper page
- Panov, A. et al. Rotenone model of Parkinson disease: multiple brain mitochondria dysfunctions after short term systemic rotenone intoxication. J. Biol. Chem. 280, 42026–42035 (2005). · DOI · Paper page
- Ludolph, A. C., He, F., Spencer, P. S., Hammerstad, J. & Sabri, M. 3-Nitropropionic acid-exogenous animal neurotoxin and possible human striatal toxin. Can. J. Neurol. Sci. 18, 492–498 (1991). · DOI
- Berridge, M. J., Bootman, M. D. & Roderick, H. L. Calcium signalling: dynamics, homeostasis and remodelling. Nature Rev. Mol. Cell Biol. 4, 517–529 (2003). · DOI
- Toescu, E. C., Verkhratsky, A. & Landfield, P. W. Ca2+ regulation and gene expression in normal brain aging. Trends Neurosci. 27, 614–620 (2004). · DOI
- Guo, Q. et al. Increased vulnerability of hippocampal neurons to excitotoxic necrosis in presenilin-1 mutant knock-in mice. Nature Med. 5, 101–106 (1999). · DOI · Paper page
- Schneider, I. et al. Mutant presenilins disturb neuronal calcium homeostasis in the brain of transgenic mice, decreasing the threshold for excitotoxicity and facilitating long-term potentiation. J. Biol. Chem. 276, 11539–11544 (2001). · DOI
- Martinez, J., Moeller, I., Erdjument-Bromage, H., Tempst, P. & Lauring, B. Parkinson's disease-associated α-synuclein is a calmodulin substrate. J. Biol. Chem. 278, 17379–17387 (2003). · DOI
- Tang, T. S. et al. Disturbed Ca2+ signaling and apoptosis of medium spiny neurons in Huntington's disease. Proc. Natl Acad. Sci. USA 102, 2602–2607 (2005). · DOI
- Smith, R. G. et al. Altered muscle calcium channel binding kinetics in autoimmune motoneuron disease. Muscle Nerve 18, 620–627 (1995). · DOI
- Von Lewinski, F. & Keller, B. U. Ca2+, mitochondria and selective motoneuron vulnerability: implications for ALS. Trends Neurosci. 28, 494–500 (2005). · DOI
- Mattson, M. P., Rychlik, B., Chu, C. & Christakos, S. Evidence for calcium-reducing and excito-protective roles for the calcium-binding protein calbindin-D28k in cultured hippocampal neurons. Neuron 6, 41–51 (1991). · DOI
- Magloczky, Z. & Freund, T. F. Selective neuronal death in the contralateral hippocampus following unilateral kainate injections into the CA3 subfield. Neuroscience 56, 317–335 (1993). · DOI
- Guela, C. et al. Loss of calbindin-D28k from aging human cholinergic basal forebrain: relation to neuronal loss. J. Comp. Neurol. 455, 249–259 (2003). · DOI
- Thorns, V., Licastro, F. & Masliah, E. Locally reduced levels of acidic FGF lead to decreased expression of 28-kDa calbindin and contribute to the selective vulnerability of the neurons in the entorhinal cortex in Alzheimer's disease. Neuropathology 21, 203–211 (2001). · DOI
- Iacopino, A. M. & Christakos, S. Specific reduction of calcium-binding protein (28-kilodalton calbindin-D) gene expression in aging and neurodegenerative diseases. Proc. Natl Acad. Sci. USA 87, 4078–4082 (1990). Evidence that age- and neuron-specific changes in calcium-binding proteins are associated with SNV. · DOI
- Alexianu, M. E. et al. The role of calcium-binding proteins in selective motoneuron vulnerability in amyotrophic lateral sclerosis. Ann. Neurol. 36, 846–858 (1994). · DOI
- Ikonomovic, M. D. et al. Distribution of glutamate receptor subunit NMDAR1 in the hippocampus of normal elderly and patients with Alzheimer's disease. Exp. Neurol. 160, 194–204 (1999). · DOI
- Williams, T. L., Day, N. C., Ince, P. G., Kamboj, R. K. & Shaw, P. J. Calcium-permeable α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors: a molecular determinant of selective vulnerability in amyotrophic lateral sclerosis. Ann. Neurol. 42, 200–207 (1997). · DOI
- Melov, S. Modeling mitochondrial function in aging neurons. Trends Neurosci. 27, 601–606 (2004). · DOI
- Petit-Taboue, M. C., Landeau, B., Desson, J. F., Desgranges, B. & Baron, J. C. Effects of healthy aging on the regional cerebral metabolic rate of glucose assessed with statistical parametric mapping. Neuroimage 7, 176–184 (1998). · DOI · Paper page
- Masconi, L. Brain glucose metabolism in the early and specific diagnosis of Alzheimer's disease. FDG-PET studies in MCI and AD. Eur. J. Nucl. Med. Mol. Imaging 32, 486–510 (2005). · DOI
- Dagher, A. Functional imaging in Parkinson's disease. Semin. Neurol. 21, 23–32 (2001). · DOI
- Feigin, A. et al. Metabolic network abnormalities in early Huntington's disease: an [18F]FDG PET study. J. Nucl. Med. 42, 1591–1595 (2001).
- Bubber, P., Haroutunian, V., Fisch, G., Blass, J. P. & Gibson, G. E. Mitochondrial abnormalities in Alzheimer brain: mechanistic implications. Ann. Neurol. 57, 695–703 (2005). · DOI · Paper page
- Smigrodzki, R., Parks, J. & Parker, W. D. High frequency of mitochondrial complex I mutations in Parkinson's disease and aging. Neurobiol. Aging 25, 1273–1281 (2004). · DOI
- Seong, I. S. et al. HD CAG repeat implicates a dominant property of huntingtin in mitochondrial energy metabolism. Hum. Mol. Genet. 14, 2871–2880 (2005). · DOI
- Manfredi, G. & Xu, Z. Mitochondrial dysfunction and its role in motor neuron degeneration in ALS. Mitochondrion 5, 77–87 (2005). · DOI
- Brown, M. R., Geddes, J. W. & Sullivan, P. G. Brain region-specific, age-related, alterations in mitochondrial responses to elevated calcium. J. Bioenerg. Biomembr. 36, 401–406 (2004). · DOI
- Murchison, D., Zawieja, D. C. & Griffith, W. H. Reduced mitochondrial buffering of voltage-gated calcium influx in aged rat basal forebrain neurons. Cell Calcium 36, 61–75 (2004). · DOI
- Kim, G. W. & Chan, P. H. Oxidative stress and neuronal DNA fragmentation mediate age-dependent vulnerability to the mitochondrial toxin, 3-nitropropionic acid, in the mouse striatum. Neurobiol. Dis. 8, 114–126 (2001). Evidence that neuronal vulnerability to mitochondrial toxins increases with advancing age. · DOI
- Patel, J. R. & Brewer, G. J. Age-related changes in neuronal glucose uptake in response to glutamate and β-amyloid. J. Neurosci. Res. 72, 527–536 (2003). · DOI
- Klivenyi, P. et al. Mice deficient in cellular glutathione peroxidase show increased vulnerability to malonate, 3-nitropropionic acid, and 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine. J. Neurosci. 20, 1–7 (2000). · DOI · Paper page
- Keller, J. N. et al. Mitochondrial manganese superoxide dismutase prevents neural apoptosis and reduces ischemic brain injury: suppression of peroxynitrite production, lipid peroxidation, and mitochondrial dysfunction. J. Neurosci. 18, 687–697 (1998). · DOI · Paper page
- Bruce-Keller, A. J., Umberger, G., McFall, R. & Mattson, M. P. Food restriction reduces brain damage and improves behavioral outcome following excitotoxic and metabolic insults. Ann. Neurol. 45, 8–15 (1999). · DOI
- Duan, W. & Mattson, M. P. Dietary restriction and 2-deoxyglucose administration improve behavioral outcome and reduce degeneration of dopaminergic neurons in models of Parkinson's disease. J. Neurosci. Res. 57, 195–206 (1999). · DOI
- Niwa, K., Kazama, K., Younkin, S. G., Carlson, G. A. & Iadecola, C. Alterations in cerebral blood flow and glucose utilization in mice overexpressing the amyloid precursor protein. Neurobiol. Dis. 9, 61–68 (2002). · DOI · Paper page
- Keller, J. N. et al. Increased sensitivity to mitochondrial toxin-induced apoptosis in neural cells expressing mutant presenilin-1 is linked to perturbed calcium homeostasis and enhanced oxyradical production. J. Neurosci. 18, 4439–4450 (1998). · DOI
- Guo, Q., Christakos, S., Robinson, N. & Mattson, M. P. Calbindin D28k blocks the proapoptotic actions of mutant presenilin 1: reduced oxidative stress and preserved mitochondrial function. Proc. Natl Acad. Sci. USA 95, 3227–3232 (1998). · DOI
- Trushina, E. et al. Mutant huntingtin impairs axonal trafficking in mammalian neurons in vivo and in vitro. Mol. Cell Biol. 24, 8195–8209 (2004). · DOI · Paper page
- Klivenyi, P. et al. Neuroprotective effects of creatine in a transgenic animal model of amyotrophic lateral sclerosis. Nature Med. 5, 347–350 (1999). · DOI · Paper page
- Tarnopolsky, M. A. & Beal, M. F. Potential for creatine and other therapies targeting cellular energy dysfunction in neurological disorders. Ann. Neurol. 49, 561–574 (2001). Reviews evidence that a cellular energy deficit has a key role in the degeneration of motor neurons in HD and ALS. · DOI
- Szweda, P. A., Camouse, M., Lundberg, K. C., Oberley, T. D. & Szweda, L. I. Aging, lipofuscin formation, and free radical-mediated inhibition of cellular proteolytic systems. Ageing Res. Rev. 2, 383–405 (2003). · DOI
- Gray, D. A. & Woulfe, J. Lipofuscin and aging: a matter of toxic waste. Sci. Aging Knowledge Environ. RE1 2 Feb 2005. · DOI
- Nixon, R. A. The calpains in aging and aging-related diseases. Ageing Res. Rev. 2, 407–418 (2003). · DOI
- Bi, X., Yong, A. P., Zhou, J., Gall, C. M. & Lynch, G. Regionally selective changes in brain lysosomes occur in the transition from young adulthood to middle age in rats. Neuroscience 97, 395–404 (2000). · DOI
- Keller, J. N., Hanni, K. B. & Markesbery, W. R. Possible involvement of proteasome inhibition in aging: implications for oxidative stress. Mech. Ageing Dev. 113, 61–70 (2000). · DOI
- Lam, Y. A. et al. Inhibition of the ubiquitin-proteasome system in Alzheimer's disease. Proc. Natl Acad. Sci. USA 97, 9902–9906 (2000). · DOI
- McNaught, K. S., Olanow, C. W., Halliwell, B., Isacson, O. & Jenner, P. Failure of the ubiquitin-proteasome system in Parkinson's disease. Nature Rev. Neurosci. 2, 589–594 (2001). · DOI · Paper page
- Sullivan, P. G. et al. Proteasome inhibition alters neural mitochondrial homeostasis and mitochondria turnover. J. Biol. Chem. 279, 20699–20707 (2004). · DOI
- Bednarski, E., Ribak, C. E. & Lynch, G. Suppression of cathepsins B and L causes a proliferation of lysosomes and the formation of meganeurites in hippocampus. J. Neurosci. 17, 4006–4021 (1997). · DOI
- Nixon, R. A. et al. Extensive involvement of autophagy in Alzheimer disease: an immuno-electron microscopy study. J. Neuropathol. Exp. Neurol. 64, 113–122 (2005). · DOI · Paper page
- Bergamini, E., Cavallini, G., Donati, A. & Gori, Z. The anti-ageing effects of caloric restriction may involve stimulation of macroautophagy and lysosomal degradation, and can be intensified pharmacologically. Biomed. Pharmacother. 57, 203–208 (2003). · DOI
- Maggio, J. E. et al. Reversible in vitro growth of Alzheimer disease β-amyloid plaques by deposition of labeled amyloid peptide. Proc. Natl Acad. Sci. USA 89, 5462–5466 (1992). · DOI
- Petkova, A. T. et al. Self-propagating, molecular-level polymorphism in Alzheimer's β-amyloid fibrils. Science 307, 262–265 (2005). Shows that subtle variations in the environment of pathogenic peptides modifies their self-propagating and neurotoxic properties. · DOI · Paper page
- Tanzi, R. E., Moir, R. D. & Wagner, S. L. Clearance of Alzheimer's Aβ peptide: the many roads to perdition. Neuron 43, 605–608 (2004).
- Goedert, M. Tau gene mutations and their effects. Mov. Disord. 12, S45–S52 (2005). · DOI
- Stoothoff, W. H. & Johnson, G. V. Tau phosphorylation: physiological and pathological consequences. Biochim. Biophys. Acta 1739, 280–297 (2005). · DOI
- Montine, T. J., Amarnath, V., Martin, M. E., Strittmatter, W. J. & Graham, D. G. E-4-hydroxy-2-nonenal is cytotoxic and cross-links cytoskeletal proteins in P19 neuroglial cultures. Am. J. Pathol. 148, 89–93 (1996).
- Moore, D. J., West, A. B., Dawson, V. L. & Dawson, T. M. Molecular pathophysiology of Parkinson's disease. Annu. Rev. Neurosci. 28, 57–87 (2005). · DOI
- Singleton, A. B. et al. α-Synuclein locus triplication causes Parkinson's disease. Science 302, 841 (2003). The first evidence that a modest increase in the production of α-synuclein is sufficient to cause PD. · DOI · Paper page
- Yavich, L., Tanila, H., Vepsalainen, S. & Jakala, P. Role of α-synuclein in presynaptic dopamine recruitment. J. Neurosci. 24, 11165–11170 (2004). · DOI
- Bates, G. Huntingtin aggregation and toxicity in Huntington's disease. Lancet 361, 1642–1644 (2003). · DOI
- Fox, J. H. et al. Cystamine increases L-cysteine levels in Huntington's disease transgenic mouse brain and in a PC12 model of polyglutamine aggregation. J. Neurochem. 91, 413–422 (2004). · DOI
- Wyttenbach, A. et al. Heat shock protein 27 prevents cellular polyglutamine toxicity and suppresses the increase of reactive oxygen species caused by huntingtin. Hum. Mol. Genet. 11, 1137–1151 (2002). · DOI
- Giffard, R. G. et al. Chaperones, protein aggregation, and brain protection from hypoxic/ischemic injury. J. Exp. Biol. 207, 3213–3220 (2004). · DOI
- Cohen, F. E. & Kelly, J. W. Therapeutic approaches to protein-misfolding diseases. Nature 426, 905–909 (2003). · DOI
- Zhao, L., Longo-Guess, C., Harris, B. S., Lee, J. W. & Ackerman, S. L. Protein accumulation and neurodegeneration in the woozy mutant mouse is caused by disruption of SIL1, a cochaperone of BiP. Nature Genet. 37, 974–979 (2005). · DOI
- Rousseau, E. et al. Targeting expression of expanded polyglutamine proteins to the endoplasmic reticulum or mitochondria prevents their aggregation. Proc. Natl Acad. Sci. USA 101, 9648–9653 (2004). · DOI
- Kieran, D. et al. Treatment with arimoclomol, a coinducer of heat shock proteins, delays disease progression in ALS mice. Nature Med. 10, 402–405 (2004). Pharmacological induction of protein chaperones results in therapeutic benefit in a mouse model of ALS. · DOI
- Siegel, G. J. & Chauhan, N. B. Neurotrophic factors in Alzheimer's and Parkinson's disease brain. Brain Res. Rev. 33, 199–227 (2000). · DOI
- Dore, S., Kar, S. & Quirion, R. Insulin-like growth factor I protects and rescues hippocampal neurons against β-amyloid- and human amylin-induced toxicity. Proc. Natl Acad. Sci. USA 94, 4772–4777 (1997). · DOI
- Counts, S. E. & Mufson, E. J. The role of nerve growth factor receptors in cholinergic basal forebrain degeneration in prodromal Alzheimer disease. J. Neuropathol. Exp. Neurol. 64, 263–272 (2005). · DOI
- Gash, D. M., Zhang, Z. & Gerhardt, G. Neuroprotective and neurorestorative properties of GDNF. Ann. Neurol. 44, S121–S125 (1998). · DOI
- Ross, C. A. Huntington's disease: new paths to pathogenesis. Cell 118, 4–7 (2004). · DOI
- Wilczak, N. & de Keyser, J. Insulin-like growth factor system in amyotrophic lateral sclerosis. Endocr. Dev. 9, 160–169 (2005). · DOI
- Hattiangady, B., Rao, M. S., Shetty, G. A. & Shetty, A. K. Brain-derived neurotrophic factor, phosphorylated cyclic AMP response element binding protein and neuropeptide Y decline as early as middle age in the dentate gyrus and CA1 and CA3 subfields of the hippocampus. Exp. Neurol. 195, 353–371 (2005). · DOI
- Gooney, M., Messaudi, E., Maher, F. O., Bramham, C. R. & Lynch, M. A. BDNF-induced LTP in dentate gyrus is impaired with age: analysis of changes in cell signaling events. Neurobiol. Aging 25, 1323–1331 (2004). · DOI
- Monti, B., Berteotti, C. & Contestabile, A. Dysregulation of memory-related proteins in the hippocampus of aged rats and their relation with cognitive impairment. Hippocampus 15, 1041–1049 (2005). · DOI
- Adlard, P. A., Perreau, V. M. & Cotman, C. W. The exercise-induced expression of BDNF within the hippocampus varies across life-span. Neurobiol. Aging 26, 511–520 (2005). · DOI · Paper page
- Yurek, D. M. & Fletcher-Turner, A. Lesion-induced increase of BDNF is greater in the striatum of young versus old rat brain. Exp. Neurol. 161, 392–396 (2000). · DOI
- Dore, S., Kar, S., Rowe, W. & Quirion, R. Distribution and levels of [125I]IGF-I, [125I]IGF-II and [125I]insulin receptor binding sites in the hippocampus of aged memory-unimpaired and -impaired rats. Neuroscience 80, 1033–1040 (1997). · DOI
- D'Costa, A. P., Xu, X., Ingram, R. L. & Sonntag, W. E. Insulin-like growth factor-1 stimulation of protein synthesis is attenuated in cerebral cortex of aging rats. Neuroscience 65, 805–813 (1995). · DOI
- Woods, A. G., Guthrie, K. M., Kurlawalla, M. A. & Gall, C. M. Deafferentation-induced increases in hippocampal insulin-like growth factor-1 messenger RNA expression are severely attenuated in middle aged and aged rats. Neuroscience 83, 663–668 (1998). Evidence that the capacity of brain cells to increase neurotrophic factor signalling is impaired during ageing. · DOI
- Sonntag, W. E., Ramsey, M. & Carter, C. S. Growth hormone and insulin-like growth factor-1 (IGF-1) and their influence on cognitive aging. Ageing Res. Rev. 4, 195–212 (2005). · DOI
- Grondin, R. et al. Glial cell line-derived neurotrophic factor increases stimulus-evoked dopamine release and motor speed in aged rhesus monkeys. J. Neurosci. 23, 1974–1980 (2003). · DOI
- Martinez-Serrano, A., Fischer, W. & Bjorklund, A. Reversal of age-dependent cognitive impairments and cholinergic neuron atrophy by NGF-secreting neural progenitors grafted to the basal forebrain. Neuron 15, 473–484 (1995). The authors show that it is possible to recover age-dependent cognitive deficits by transplantation of neurotrophic factor-producing cells into the basal forebrain. · DOI
- Lopez-Lopez, C., LeRoith, D. & Torres-Aleman, I. Insulin-like growth factor I is required for vessel remodeling in the adult brain. Proc. Natl Acad. Sci. USA 101, 9833–9838 (2004). · DOI · Paper page
- Murer, M. G., Yan, Q. & Raisman-Vozari, R. Brain-derived neurotrophic factor in the control human brain, and in Alzheimer's disease and Parkinson's disease. Prog. Neurobiol. 63, 71–124 (2001). · DOI · Paper page
- Scott, S. A. & Crutcher, K. A. Nerve growth factor and Alzheimer's disease. Rev. Neurosci. 5, 179–211 (1994). · DOI
- Zuccato, C. et al. Loss of huntingtin-mediated BDNF gene transcription in Huntington's disease. Science 293, 493–498 (2001). The first evidence that mutant huntingtin perturbs transcriptional regulation of neurotrophic factor production. · DOI · Paper page
- Duan, W. et al. Paroxetine retards disease onset and progression in Huntingtin mutant mice. Ann. Neurol. 55, 590–594 (2004). · DOI
- Dehmelt, L. & Halpain, S. The MAP2/Tau family of microtubule-associated proteins. Genome Biol. 6, 204 (2005). · DOI · Paper page
- Al-Chalabi, A. & Miller, C. C. Neurofilaments and neurological disease. Bioessays 25, 346–355 (2003). · DOI
- Trojanowski, J. Q. & Lee, V. M. The role of tau in Alzheimer's disease. Med. Clin. North Am. 86, 615–627 (2002). · DOI · Paper page
- Norris, E. H. & Giasson, B. I. Role of oxidative damage in protein aggregation associated with Parkinson's disease and related disorders. Antioxid. Redox Signal. 7, 672–684 (2005). · DOI
- O'Neill, C. et al. Dysfunctional intracellular calcium homoeostasis: a central cause of neurodegeneration in Alzheimer's disease. Biochem. Soc. Symp. 67, 177–194 (2001). · DOI
- Gauthier, L. R. et al. Huntingtin controls neurotrophic support and survival of neurons by enhancing BDNF vesicular transport along microtubules. Cell 118, 127–138 (2004). · DOI · Paper page
- Zhang, B., Tu, P., Abtahian, F. & Trojanowski, J. Q. Neurofilaments and orthograde transport are reduced in ventral root axons of transgenic mice that express human SOD1 with a G93A mutation. J. Cell Biol. 139, 1307–1315 (1997). Reports direct evidence that a mutation that causes ALS impairs axonal transport in motor neurons. · DOI
- Ishihara, T. et al. Age-dependent emergence and progression of a tauopathy in transgenic mice overexpressing the shortest human tau isoform. Neuron 24, 751–762 (1999). · DOI · Paper page
- Brandt, R., Hundelt, M. & Shahani, N. Tau alteration and neuronal degeneration in tauopathies: mechanisms and models. Biochim. Biophys. Acta 1739, 331–354 (2005). · DOI
- McGeer, P. L. & McGeer, E. G. Local neuroinflammation and the progression of Alzheimer's disease. J. Neurovirol. 8, 529–538 (2002). · DOI
- Dickson, D. W., Lee, S. C., Mattiace, L. A., Yen, S. H. & Brosnan, C. Microglia and cytokines in neurological disease, with special reference to AIDS and Alzheimer's disease. Glia 7, 75–83 (1993). · DOI
- Eikelenboom, P., Hack, C. E., Rozemuller, J. M. & Stam, F. C. Complement activation in amyloid plaques in Alzhiemer's dementia. Virchows Arch. 56, 259–262 (1989). · DOI
- Nath, A. et al. Autoantibodies to amyloid β-peptide (Aβ) are increased in Alzheimer's disease patients and Aβ antibodies can enhance Aβ neurotoxicity: implications for disease pathogenesis and vaccine development. Neuromolecular Med. 3, 29–39 (2003). · DOI
- Teismann, P. & Schulz, J. B. Cellular pathology of Parkinson's disease: astrocytes, microglia and inflammation. Cell Tissue Res. 318, 149–161 (2004). · DOI
- Sargsyan, S. A., Monk, P. N. & Shaw, P. J. Microglia as potential contributors to motor neuron injury in amyotrophic lateral sclerosis. Glia 51, 241–253 (2005). · DOI
- Smith, R. G. et al. Cytotoxicity of immunoglobulins from amyotrophic lateral sclerosis patients on a hybrid motoneuron cell line. Proc. Natl Acad. Sci. USA 91, 3393–3397 (1994). · DOI
- Miller, R. G., Mitchell, J. D., Lyon, M. & Moore, D. H. Riluzole for amyotrophic lateral sclerosis (ALS)/motor neuron disease (MND). Amyotroph. Lateral Scler. Other Motor Neuron Disord. 4, 191–206 (2003). · DOI
- Reisberg, B. et al. A 24-week open-label extension study of memantine in moderate to severe Alzheimer disease. Arch. Neurol. 63, 49–54 (2006). · DOI
- Wang, J. et al. Caloric restriction attenuates β-amyloid neuropathology in a mouse model of Alzheimer's disease. FASEB J. 19, 659–661 (2005). · DOI
- Lazarov, O. et al. Environmental enrichment reduces Aβ levels and amyloid deposition in transgenic mice. Cell 120, 701–713 (2005). Reports the first evidence that exercise/cognitive stimulation can enhance clearance of Aβ from the brain. · DOI · Paper page
- Lim, G. P. et al. A diet enriched with the ω-3 fatty acid docosahexaenoic acid reduces amyloid burden in an aged Alzheimer mouse model. J. Neurosci. 25, 3032–3040 (2005). · DOI
- DeKosky, S. T. Statin therapy in the treatment of Alzheimer disease: what is the rationale? Am. J. Med. 118, S48–S53 (2005). · DOI
- Lipton, S. A. Paradigm shift in NMDA receptor antagonist drug development: molecular mechanism of uncompetitive inhibition by memantine in the treatment of Alzheimer's disease and other neurologic disorders. J. Alzheimers Dis. 6, S61–S74 (2004). · DOI · Paper page
- Duan, W. et al. p53 inhibitors preserve dopamine neurons and motor function in experimental parkinsonism. Ann. Neurol. 52, 597–606 (2002). · DOI
- Bae, B. I. et al. p53 mediates cellular dysfunction and behavioral abnormalities in Huntington's disease. Neuron 47, 29–41 (2005). · DOI
- Ellis, A. C. & Rosenfeld, J. The role of creatine in the management of amyotrophic lateral sclerosis and other neurodegenerative disorders. CNS Drugs 18, 967–980 (2004). · DOI
- Kordower, J. H. et al. Neurodegeneration prevented by lentiviral vector delivery of GDNF in primate models of Parkinson's disease. Science 290, 767–773 (2000). Reports the efficacy of gene therapy in a non-human primate model of PD. · DOI
- Dobrowolny, G. et al. Muscle expression of a local IGF-1 isoform protects motor neurons in an ALS mouse model. J. Cell Biol. 168, 193–199 (2005). · DOI
- Levy, Y. S., Gilgun-Sherki, Y., Melamed, E. & Offen, D. Therapeutic potential of neurotrophic factors in neurodegenerative diseases. BioDrugs 19, 97–127 (2005). · DOI
- Gelinas, D. S., DaSilva, K., Fenili, D., St Georger-Hyslop, P. & McLaurin, J. Immunotherapy for Alzheimer's disease. Proc. Natl Acad. Sci. USA 101, S14657–S14662 (2004). · DOI
- Harper, S. Q. et al. RNA interference improves motor and neuropathological abnormalities in a Huntington's disease mouse model. Proc. Natl Acad. Sci. USA 102, 5820–5825 (2005). · DOI · Paper page
200 of 212 shown
Cited by
Sorted by citations
Oxidative Stress, Synaptic Dysfunction, and Alzheimer’s Disease
Tönnies, E., & Trushina, E. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-161088 · Cited by 1,750
Normal aging induces A1-like astrocyte reactivity
Clarke, L. E., Liddelow, S. A., Chakraborty, C., Münch, A. E., Heiman, M., & Barres, B. A. (2018) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1800165115 · Cited by 1,237
Targeting Antioxidants to Mitochondria by Conjugation to Lipophilic Cations
Murphy, M. P., & Smith, R. A. J. (2007) · Annual Review of Pharmacology and Toxicology · doi:10.1146/annurev.pharmtox.47.120505.105110 · Cited by 1,173
Young blood reverses age-related impairments in cognitive function and synaptic plasticity in mice
Villeda, S. A., Plambeck, K. E., Middeldorp, J., Castellano, J. M., Mosher, K. I., Luo, J., Smith, L. K., Bieri, G., Lin, K., Berdnik, D., et al. (2014) · Nature Medicine · doi:10.1038/nm.3569 · Cited by 1,081
The cholinergic system in aging and neuronal degeneration
Schliebs, R., & Arendt, T. (2011) · Behavioural Brain Research · doi:10.1016/j.bbr.2010.11.058 · Cited by 1,047
Cell death by necrosis: towards a molecular definition
Golstein, P., & Kroemer, G. (2007) · Trends in Biochemical Sciences · doi:10.1016/j.tibs.2006.11.001 · Cited by 1,044
Neuronal calcium mishandling and the pathogenesis of Alzheimer's disease
Bezprozvanny, I., & Mattson, M. P. (2008) · Trends in Neurosciences · doi:10.1016/j.tins.2008.06.005 · Cited by 938
Self-citationMattson, M. P. (2007) · Aging Cell · doi:10.1111/j.1474-9726.2007.00275.x · Cited by 751
Self-citationThe neuroscience of socioeconomic status: Correlates, causes, and consequences
Farah, M. J. (2017) · Neuron · doi:10.1016/j.neuron.2017.08.034 · Cited by 653
Glutamate and Neurotrophic Factors in Neuronal Plasticity and Disease
Mattson, M. P. (2008) · Annals of the New York Academy of Sciences · doi:10.1196/annals.1418.005 · Cited by 640
Self-citationExercise, oxidative stress and hormesis
Radak, Z., Chung, H. Y., Koltai, E., Taylor, A. W., & Goto, S. (2008) · Ageing Research Reviews · doi:10.1016/j.arr.2007.04.004 · Cited by 638
Systemic adaptation to oxidative challenge induced by regular exercise
Radak, Z., Chung, H. Y., & Goto, S. (2008) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2007.01.029 · Cited by 623
Aging-induced type I interferon response at the choroid plexus negatively affects brain function
Baruch, K., Deczkowska, A., David, E., Castellano, J. M., Miller, O., Kertser, A., Berkutzki, T., Barnett-Itzhaki, Z., Bezalel, D., Wyss-Coray, T., et al. (2014) · Science · doi:10.1126/science.1252945 · Cited by 615
Selective vulnerability in neurodegenerative diseases
Fu, H., Hardy, J., & Duff, K. E. (2018) · Nature Neuroscience · doi:10.1038/s41593-018-0221-2 · Cited by 585
β2-microglobulin is a systemic pro-aging factor that impairs cognitive function and neurogenesis
Smith, L. K., He, Y., Park, J.-S., Bieri, G., Snethlage, C. E., Lin, K., Gontier, G., Wabl, R., Plambeck, K. E., Udeochu, J., et al. (2015) · Nature Medicine · doi:10.1038/nm.3898 · Cited by 500
Small molecule BDNF mimetics activate TrkB signaling and prevent neuronal degeneration in rodents
Massa, S. M., Yang, T., Xie, Y., Shi, J., Bilgen, M., Joyce, J. N., Nehama, D., Rajadas, J., & Longo, F. M. (2010) · Journal of Clinical Investigation · doi:10.1172/jci41356 · Cited by 406
Neuronal Cell Death Mechanisms in Major Neurodegenerative Diseases
Chi, H., Chang, H.-Y., & Sang, T.-K. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19103082 · Cited by 412
Spatial correlation between brain aerobic glycolysis and amyloid-β (Aβ) deposition
Vlassenko, A. G., Vaishnavi, S. N., Couture, L., Sacco, D., Shannon, B. J., Mach, R. H., Morris, J. C., Raichle, M. E., & Mintun, M. A. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1010461107 · Cited by 404
Mitochondrion-derived reactive oxygen species lead to enhanced amyloid beta formation
Leuner, K., Schütt, T., Kurz, C., Eckert, S. H., Schiller, C., Occhipinti, A., Mai, S., Jendrach, M., Eckert, G. P., Kruse, S. E., et al. (2012) · Antioxidants & Redox Signaling · doi:10.1089/ars.2011.4173 · Cited by 354
Marlatt, M. W., Potter, M. C., Lucassen, P. J., & van Praag, H. (2012) · Developmental Neurobiology · doi:10.1002/dneu.22009 · Cited by 314
Locus coeruleus cellular and molecular pathology during the progression of Alzheimer’s disease
Kelly, S. C., He, B., Perez, S. E., Ginsberg, S. D., Mufson, E. J., & Counts, S. E. (2017) · Acta Neuropathologica Communications · doi:10.1186/s40478-017-0411-2 · Cited by 286
Female Sex and Alzheimer's Risk: The Menopause Connection
Scheyer, O., Rahman, A., Hristov, H., Berkowitz, C., Isaacson, R. S., Diaz Brinton, R., & Mosconi, L. (2018) · The Journal of Prevention of Alzheimer's Disease · doi:10.14283/jpad.2018.34 · Cited by 268
Hyun, D.-H., Emerson, S. S., Jo, D.-G., Mattson, M. P., & de Cabo, R. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0608008103 · Cited by 267
Self-citationAutophagy Is Required for Memory Formation and Reverses Age-Related Memory Decline
Glatigny, M., Moriceau, S., Rivagorda, M., Ramos-Brossier, M., Nascimbeni, A. C., Lante, F., Shanley, M. R., Boudarene, N., Rousseaud, A., Friedman, A. K., et al. (2019) · Current Biology · doi:10.1016/j.cub.2018.12.021 · Cited by 257
Aging‐dependent changes of microglial cells and their relevance for neurodegenerative disorders
Von Bernhardi, R., Tichauer, J. E., & Eugenín, J. (2010) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2009.06537.x · Cited by 258
Senatorov, V. V., Friedman, A. R., Milikovsky, D. Z., Ofer, J., Saar-Ashkenazy, R., Charbash, A., Jahan, N., Chin, G., Mihaly, E., Lin, J. M., et al. (2019) · Science Translational Medicine · doi:10.1126/scitranslmed.aaw8283 · Cited by 257
Brain Endothelial Cells Are Exquisite Sensors of Age-Related Circulatory Cues
Chen, M. B., Yang, A. C., Yousef, H., Lee, D., Chen, W., Schaum, N., Lehallier, B., Quake, S. R., & Wyss-Coray, T. (2020) · Cell Reports · doi:10.1016/j.celrep.2020.03.012 · Cited by 233
“Aging drives the deterioration of brain structure and function, increasing susceptibility to neurodegenerative disease and cognitive decline (Andrews-Hanna et al., 2007; Bishop et al., 2010; Mattson and Magnus, 2006).”
Age-dependent instability of mature neuronal fate in induced neurons from Alzheimer’s patients
Mertens, J., Herdy, J. R., Traxler, L., Schafer, S. T., Schlachetzki, J. C. M., Böhnke, L., Reid, D. A., Lee, H., Zangwill, D., Fernandes, D. P., et al. (2021) · Cell Stem Cell · doi:10.1016/j.stem.2021.04.004 · Cited by 240
Prevention of dementia in an ageing world: Evidence and biological rationale
Grande, G., Qiu, C., & Fratiglioni, L. (2020) · Ageing Research Reviews · doi:10.1016/j.arr.2020.101045 · Cited by 229
Perluigi, M., Coccia, R., & Butterfield, D. A. (2012) · Antioxidants & Redox Signaling · doi:10.1089/ars.2011.4406 · Cited by 229
Changes in Regenerative Capacity through Lifespan
Yun, M. (2015) · International Journal of Molecular Sciences · doi:10.3390/ijms161025392 · Cited by 216
Maintenance of age in human neurons generated by microRNA-based neuronal conversion of fibroblasts
Huh, C. J., Zhang, B., Victor, M. B., Dahiya, S., Batista, L. F., Horvath, S., & Yoo, A. S. (2016) · eLife · doi:10.7554/elife.18648 · Cited by 213
“DOI: 10.7554/eLife.18648 1 of 14 SHORT REPORT modeling early developmental phenotypes (Lafaille et al., 2012; Lee et al., 2009), iPSC-derived cells have been reported to be unsuitable in recapitulating phenotypes selectively observed in aged cells (Mattson and Magnus, 2006; Vera and Studer, 2015).”
BackgroundMethodInfluentialStranahan, A. M., & Mattson, M. P. (2010) · Neural Plasticity · doi:10.1155/2010/108190 · Cited by 198
“Within the entorhinal cortex, neurons in layer II are particularly susceptible to the deleterious consequences of aging, MCI, and AD [5], but”
BackgroundSelf-citationHerdy, J. R., Traxler, L., Agarwal, R. K., Karbacher, L., Schlachetzki, J. C. M., Boehnke, L., Zangwill, D., Galasko, D., Glass, C. K., Mertens, J., et al. (2022) · Cell Stem Cell · doi:10.1016/j.stem.2022.11.010 · Cited by 208
Ryan, N. S., Keihaninejad, S., Shakespeare, T. J., Lehmann, M., Crutch, S. J., Malone, I. B., Thornton, J. S., Mancini, L., Hyare, H., Yousry, T., et al. (2013) · Brain · doi:10.1093/brain/awt065 · Cited by 205
Metabolomics of Human Brain Aging and Age-Related Neurodegenerative Diseases
Jové, M., Portero-Otín, M., Naudí, A., Ferrer, I., & Pamplona, R. (2014) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0000000000000091 · Cited by 195
Dysregulated neuronal–microglial cross-talk during aging, stress and inflammation
Jurgens, H. A., & Johnson, R. W. (2012) · Experimental Neurology · doi:10.1016/j.expneurol.2010.11.014 · Cited by 179
Del Arco, A., & Mora, F. (2008) · Pharmacology Biochemistry and Behavior · doi:10.1016/j.pbb.2008.04.011 · Cited by 163
Brain cholesterol in normal and pathological aging
Martin, M., Dotti, C. G., & Ledesma, M. D. (2010) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2010.03.011 · Cited by 162
Age mosaicism across multiple scales in adult tissues
Arrojo e Drigo, R., Lev-Ram, V., Tyagi, S., Ramachandra, R., Deerinck, T., Bushong, E., Phan, S., Orphan, V., Lechene, C., Ellisman, M. H., et al. (2019) · Cell Metabolism · doi:10.1016/j.cmet.2019.05.010 · Cited by 137
Krystal, J. H., Abdallah, C. G., Averill, L. A., Kelmendi, B., Harpaz-Rotem, I., Sanacora, G., Southwick, S. M., & Duman, R. S. (2017) · Current Psychiatry Reports · doi:10.1007/s11920-017-0829-z · Cited by 145
Silaidos, C., Pilatus, U., Grewal, R., Matura, S., Lienerth, B., Pantel, J., & Eckert, G. P. (2018) · Biology of Sex Differences · doi:10.1186/s13293-018-0193-7 · Cited by 137
Incorporation of a nucleoside analog maps genome repair sites in postmitotic human neurons
Reid, D. A., Reed, P. J., Schlachetzki, J. C. M., Nitulescu, I. I., Chou, G., Tsui, E. C., Jones, J. R., Chandran, S., Lu, A. T., McClain, C. A., et al. (2021) · Science · doi:10.1126/science.abb9032 · Cited by 121
Gan, K. J., & Südhof, T. C. (2019) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1902672116 · Cited by 114
Vilela, T. C., Muller, A. P., Damiani, A. P., Macan, T. P., da Silva, S., Canteiro, P. B., de Sena Casagrande, A., Pedroso, G. D. S., Nesi, R. T., de Andrade, V. M., et al. (2017) · Molecular Neurobiology · doi:10.1007/s12035-016-0272-x · Cited by 115
Neuronal O-GlcNAcylation Improves Cognitive Function in the Aged Mouse Brain
Wheatley, E. G., Albarran, E., White, C. W., Bieri, G., Sanchez-Diaz, C., Pratt, K., Snethlage, C. E., Ding, J. B., & Villeda, S. A. (2019) · Current Biology · doi:10.1016/j.cub.2019.08.003 · Cited by 107
Does exercise reduce brain oxidative stress? A systematic review
Camiletti‐Moirón, D., Aparicio, V. A., Aranda, P., & Radak, Z. (2013) · Scandinavian Journal of Medicine & Science in Sports · doi:10.1111/sms.12065 · Cited by 104
Xu, J., Begley, P., Church, S. J., Patassini, S., McHarg, S., Kureishy, N., Hollywood, K. A., Waldvogel, H. J., Liu, H., Zhang, S., et al. (2016) · Scientific Reports · doi:10.1038/srep27524 · Cited by 85
Comparative Proteomic Analysis of Brains of Naturally Aging Mice
Yang, S., Liu, T., Li, S., Zhang, X., Ding, Q., Que, H., Yan, X., Wei, K., & Liu, S. (2008) · Neuroscience · doi:10.1016/j.neuroscience.2008.04.012 · Cited by 82
Role of glucagon-like peptide-1 receptor agonists in Alzheimer’s disease and Parkinson’s disease
Hong, C.-T., Chen, J.-H., & Hu, C.-J. (2024) · Journal of Biomedical Science · doi:10.1186/s12929-024-01090-x · Cited by 78
Integrative neurobiology of metabolic diseases, neuroinflammation, and neurodegeneration
van Dijk, G., van Heijningen, S., Reijne, A. C., Nyakas, C., van der Zee, E. A., & Eisel, U. L. M. (2015) · Frontiers in Neuroscience · doi:10.3389/fnins.2015.00173 · Cited by 75
Shen, Y., Tian, M., Zheng, Y., Gong, F., Fu, A. K. Y., & Ip, N. Y. (2016) · Cell Reports · doi:10.1016/j.celrep.2016.10.043 · Cited by 67
Alkhalifa, A. E., Alkhalifa, O., Durdanovic, I., Ibrahim, D. R., & Maragkou, S. (2025) · Journal of Dementia and Alzheimer's Disease · doi:10.3390/jdad2020017 · Cited by 66
Park, M. H., Jin, H. K., & Bae, J.-S. (2020) · Experimental & Molecular Medicine · doi:10.1038/s12276-020-0399-8 · Cited by 59
Del Arco, A., Segovia, G., de Blas, M., Garrido, P., Acuña-Castroviejo, D., Pamplona, R., & Mora, F. (2011) · Behavioural Brain Research · doi:10.1016/j.bbr.2010.07.024 · Cited by 57
Clarke, G. J. B., Skandsen, T., Zetterberg, H., Einarsen, C. E., Feyling, C., Follestad, T., Vik, A., Blennow, K., & Håberg, A. K. (2021) · Frontiers in Neurology · doi:10.3389/fneur.2021.643743 · Cited by 43
The progeroid gene BubR1 regulates axon myelination and motor function
Choi, C.-I., Yoo, K. H., Hussaini, S. M. Q., Jeon, B. T., Welby, J., Gan, H., Scarisbrick, I. A., Zhang, Z., Baker, D. J., van Deursen, J. M., et al. (2016) · Aging · doi:10.18632/aging.101032 · Cited by 26
Senescence in aging and disorders of the central nervous system
Swenson, B. L., Meyer, C. F., Bussian, T. J., & Baker, D. J. (2019) · Translational Medicine of Aging · doi:10.1016/j.tma.2019.01.002 · Cited by 24
A primary cilia-autophagy axis in hippocampal neurons is essential to maintain cognitive resilience
Rivagorda, M., Romeo-Guitart, D., Blanchet, V., Mailliet, F., Boitez, V., Barry, N., Milunov, D., Siopi, E., Goudin, N., Moriceau, S., et al. (2025) · Nature Aging · doi:10.1038/s43587-024-00791-0 · Cited by 24
Tashiro, R., Ozaki, D., Bautista-Garrido, J., Sun, G., Obertas, L., Mobley, A. S., Kim, G. S., Aronowski, J., & Jung, J. E. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24065187 · Cited by 15
MT1-MMP inhibition rejuvenates ageing brain and rescues cognitive deficits in obesity
Asthana, P., Li, L., Lu, L., Wu, J., Zhang, S., Li, N., Wong, S. K. K., Gurung, S., Zhang, Y., Lin, Y., et al. (2025) · Cell Discovery · doi:10.1038/s41421-025-00825-w · Cited by 4
Metadata
- Authors
- Mattson, M. P., & Magnus, T.
- Venue
- Nature Reviews Neuroscience
- Published
- 2006-04
- Volume
- 7
- Issue
- 4
- Pages
- 278-294
- ISSN
- 1471-003X
- 1471-0048
- Cited by
- 957
- References
- 14
- Language
- en
- Licence
- www.springer.com/tdm (tdm)
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review