A network dysfunction perspective on neurodegenerative diseases (original) (raw)

• Cowan, W. M. & Kandel, E. R. Prospects for neurology and psychiatry. J. Am. Med. Assoc. 285, 594–600 (2001).
  CAS Google Scholar
• Bradshaw, J., Saling, M., Hopwood, M., Anderson, V. & Brodtmann, A. Fluctuating cognition in dementia with Lewy bodies and Alzheimer's disease is qualitatively distinct. J. Neurol. Neurosurg. Psychiatry 75, 382–387 (2004).
  CAS PubMed PubMed Central Google Scholar
• Walker, M. P. et al. The clinician assessment of fluctuation and the one day fluctuation assessment scale. Two methods to assess fluctuating confusion in dementia. Br. J. Psychiatry 177, 252–256 (2000).
  CAS PubMed Google Scholar
• Walker, M. P. et al. Quantifying fluctuation in dementia with Lewy bodies, Alzheimer's disease, and vascular dementia. Neurology 54, 1616–1625 (2000).
  CAS PubMed Google Scholar
• McKeith, I. G. et al. Diagnosis and management of dementia with Lewy bodies: third report of the DLB Consortium. Neurology 65, 1863–1872 (2005).
  CAS PubMed Google Scholar
• Robertsson, B., Blennow, K., Gottfries, C. G. & Wallin, A. Delirium in dementia. Int. J. Geriatr. Psychiatry 13, 49–56 (1998).
  CAS PubMed Google Scholar
• Terry, R. D. et al. Physical basis of cognitive alterations in Alzheimer's disease: synapse loss is the major correlate of cognitive impairment. Ann. Neurol. 30, 572–580 (1991).
  CAS PubMed Google Scholar
• Morrison, J. H. & Hof, P. R. Life and death of neurons in the aging brain. Science 278, 412–419 (1997).
  ADS CAS PubMed Google Scholar
• Kordower, J. H. et al. Loss and atrophy of layer II entorhinal cortex neurons in elderly people with mild cognitive impairment. Ann. Neurol. 49, 202–213 (2001).
  CAS PubMed Google Scholar
• Price, J. L. et al. Neuron number in the entorhinal cortex and CA1 in preclinical Alzheimer disease. Arch. Neurol. 58, 1395–1402 (2001).
  CAS PubMed Google Scholar
• Greffard, S. et al. Motor score of the Unified Parkinson Disease Rating Scale as a good predictor of Lewy body-associated neuronal loss in the substantia nigra. Arch. Neurol. 63, 584–588 (2006).
  PubMed Google Scholar
• Blanchet, P. J. Antipsychotic drug-induced movement disorders. Can. J. Neurol. Sci. 30 (Suppl. 1), S101–S107 (2003).
  PubMed Google Scholar
• Martino, D. & Giovannoni, G. Antibasal ganglia antibodies and their relevance to movement disorders. Curr. Opin. Neurol. 17, 425–432 (2004).
  PubMed Google Scholar
• Lewin, R. Is your brain really necessary? Science 210, 1232–1234 (1980).
  ADS CAS PubMed Google Scholar
• Chen, R., Cohen, L. G. & Hallett, M. Nervous system reorganization following injury. Neuroscience 111, 761–773 (2002).
  CAS PubMed Google Scholar
• Bezard, E., Gross, C. E. & Brotchie, J. M. Presymptomatic compensation in Parkinson's disease is not dopamine-mediated. Trends Neurosci. 26, 215–221 (2003).
  CAS PubMed Google Scholar
• Stern, Y. What is cognitive reserve? Theory and research application of the reserve concept. J. Int. Neuropsychol. Soc. 8, 448–460 (2002).
  PubMed Google Scholar
• Buckner, R. L. Memory and executive function in aging and AD: multiple factors that cause decline and reserve factors that compensate. Neuron 44, 195–208 (2004).
  CAS PubMed Google Scholar
• Iaria, G., Petrides, M., Dagher, A., Pike, B. & Bohbot, V. D. Cognitive strategies dependent on the hippocampus and caudate nucleus in human navigation: variability and change with practice. J. Neurosci. 23, 5945–5952 (2003).
  CAS PubMed PubMed Central Google Scholar
• Maguire, E. A., Valentine, E. R., Wilding, J. M. & Kapur, N. Routes to remembering: the brains behind superior memory. Nature Neurosci. 6, 90–95 (2003).
  CAS PubMed Google Scholar
• Mahley, R. W., Weisgraber, K. H. & Huang, Y. Apolipoprotein E4: a causative factor and therapeutic target in neuropathology, including Alzheimer's disease. Proc. Natl Acad. Sci. USA 103, 5644–5651 (2006).
  ADS CAS PubMed PubMed Central Google Scholar
• Zlokovic, B. V. Neurovascular mechanisms of Alzheimer's neurodegeneration. Trends Neurosci. 28, 202–208 (2005).
  CAS PubMed Google Scholar
• Prinz, A. A., Bucher, D. & Marder, E. Similar network activity from disparate circuit parameters. Nature Neurosci. 7, 1345–1352 (2004).
  CAS PubMed Google Scholar
• Edelman, G. M. & Gally, J. A. Degeneracy and complexity in biological systems. Proc. Natl Acad. Sci. USA 98, 13763–13768 (2001).
  ADS CAS PubMed PubMed Central Google Scholar
• Whone, A. L., Moore, R. Y., Piccini, P. P. & Brooks, D. J. Plasticity of the nigropallidal pathway in Parkinson's disease. Ann. Neurol. 53, 206–213 (2003).
  PubMed Google Scholar
• Walsh, D. M. & Selkoe, D. J. Deciphering the molecular basis of memory failure in Alzheimer's disease. Neuron 44, 181–193 (2004).
  CAS PubMed Google Scholar
• Muchowski, P. J. & Wacker, J. L. Modulation of neurodegeneration by molecular chaperones. Nature Rev. Neurosci. 6, 11–22 (2005).
  CAS Google Scholar
• Mark, R. J., Ashford, J. W., Goodman, Y. & Mattson, M. P. Anticonvulsants attenuate amyloid β-peptide neurotoxicity, Ca2+ deregulation, and cytoskeletal pathology. Neurobiol. Aging 16, 187–198 (1995).
  CAS PubMed Google Scholar
• Hynd, M. R., Scott, H. L. & Dodd, P. R. Glutamate-mediated excitotoxicity and neurodegeneration in Alzheimer's disease. Neurochem. Int. 45, 583–595 (2004).
  CAS PubMed Google Scholar
• Wyss-Coray, T. & Mucke, L. Inflammation in neurodegenerative disease — a double-edged sword. Neuron 35, 419–432 (2002).
  CAS PubMed Google Scholar
• Beal, M. F. Mitochondria take center stage in aging and neurodegeneration. Ann. Neurol. 58, 495–505 (2005).
  CAS PubMed Google Scholar
• Small, D. H., Mok, S. S. & Bornstein, J. C. Alzheimer's disease and Aβ toxicity: from top to bottom. Nature Rev. Neurosci. 2, 595–598 (2001).
  CAS Google Scholar
• Mattson, M. P. Pathways towards and away from Alzheimer's disease. Nature 430, 631–639 (2004).
  ADS CAS PubMed PubMed Central Google Scholar
• Handley, O. J., Naji, J. J., Dunnett, S. B. & Rosser, A. E. Pharmaceutical, cellular and genetic therapies for Huntington's disease. Clin. Sci. (Lond.) 110, 73–88 (2006).
  CAS Google Scholar
• Honer, W. G. Pathology of presynaptic proteins in Alzheimer's disease: more than simple loss of terminals. Neurobiol. Aging 24, 1047–1062 (2003).
  CAS PubMed Google Scholar
• Levine, M. S., Cepeda, C., Hickey, M. A., Fleming, S. M. & Chesselet, M. F. Genetic mouse models of Huntington's and Parkinson's diseases: illuminating but imperfect. Trends Neurosci. 27, 691–697 (2004).
  CAS PubMed Google Scholar
• van Dellen, A., Grote, H. E. & Hannan, A. J. Gene–environment interactions, neuronal dysfunction and pathological plasticity in Huntington's disease. Clin. Exp. Pharmacol. Physiol. 32, 1007–1019 (2005).
  CAS PubMed Google Scholar
• Lazarov, O. et al. Environmental enrichment reduces Aβ levels and amyloid deposition in transgenic mice. Cell 120, 701–713 (2005).
  CAS PubMed Google Scholar
• Mesulam, M. M. Neuroplasticity failure in Alzheimer's disease: bridging the gap between plaques and tangles. Neuron 24, 521–529 (1999).
  CAS PubMed Google Scholar
• Verdier, Y., Zarandi, M. & Penke, B. Amyloid β-peptide interactions with neuronal and glial cell plasma membrane: binding sites and implications for Alzheimer's disease. J. Pept. Sci. 10, 229–248 (2004).
  CAS PubMed Google Scholar
• Schmitt, H. P. Pouring oil into the fire? On the conundrum of the beneficial effects of NMDA receptor antagonists in Alzheimer disease. Psychopharmacology (Berl.) 9, 151–153 (2005).
  ADS Google Scholar
• Chen, J. et al. SIRT1 protects against microglia-dependent amyloid-β toxicity through inhibiting NF-κB signaling. J. Biol. Chem. 280, 40364–40374 (2005).
  CAS PubMed Google Scholar
• Giorgini, F., Guidetti, P., Nguyen, Q., Bennett, S. C. & Muchowski, P. J. A genomic screen in yeast implicates kynurenine 3-monooxygenase as a therapeutic target for Huntington disease. Nature Genet. 37, 526–531 (2005).
  CAS PubMed Google Scholar
• Eddleston, M. P. & Mucke, L. Molecular profile of reactive astrocytes — implications for their role in neurologic disease. Neuroscience 54, 15–36 (1993).
  CAS PubMed Google Scholar
• Palop, J. J. et al. Neuronal depletion of calcium-dependent proteins in the dentate gyrus is tightly linked to Alzheimer's disease-related cognitive deficits. Proc. Natl Acad. Sci. USA 100, 9572–9577 (2003).
  ADS CAS PubMed PubMed Central Google Scholar
• Drzezga, A. et al. Impaired cross-modal inhibition in Alzheimer disease. PLoS Med. 2, 986–995 (2005).
  Google Scholar
• Palop, J. J. et al. Vulnerability of dentate granule cells to disruption of Arc expression in human amyloid precursor protein transgenic mice. J. Neurosci. 25, 9686–9693 (2005).
  CAS PubMed PubMed Central Google Scholar
• Colom, L. V. Septal networks: relevance to theta rhythm, epilepsy and Alzheimer's disease. J. Neurochem. 96, 609–623 (2006).
  CAS PubMed Google Scholar
• Arrasate, M., Mitra, S., Schweitzer, E. S., Segal, M. R. & Finkbeiner, S. Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death. Nature 431, 805–810 (2004).
  ADS CAS PubMed Google Scholar
• Graf, R. A. & Kater, S. B. Inhibitory neuronal activity can compensate for adverse effects of β-amyloid in hippocampal neurons. Brain Res. 786, 115–121 (1998).
  CAS PubMed Google Scholar
• Watanabe, D. et al. Ablation of cerebellar Golgi cells disrupts synaptic integration involving GABA inhibition and NMDA receptor activation in motor coordination. Cell 95, 17–27 (1998).
  CAS PubMed Google Scholar
• DeKosky, S. T. et al. Upregulation of choline acetyltransferase activity in hippocampus and frontal cortex of elderly subjects with mild cognitive impairment. Ann. Neurol. 51, 145–155 (2002).
  CAS PubMed Google Scholar
• Small, D. H. Do acetylcholinesterase inhibitors boost synaptic scaling in Alzheimer's disease? Trends Neurosci. 27, 245–249 (2004).
  CAS PubMed Google Scholar
• Dickerson, B. C. et al. Increased hippocampal activation in mild cognitive impairment compared to normal aging and AD. Neurology 65, 404–411 (2005).
  CAS PubMed Google Scholar
• Oldstone, M. B. Molecular mimicry, microbial infection, and autoimmune disease: evolution of the concept. Curr. Top. Microbiol. Immunol. 296, 1–17 (2005).
  CAS PubMed PubMed Central Google Scholar
• Duncan, J. S., Sander, J. W., Sisodiya, S. M. & Walker, M. C. Adult epilepsy. Lancet 367, 1087–1100 (2006).
  PubMed Google Scholar
• Thompson, P. J. & Duncan, J. S. Cognitive decline in severe intractable epilepsy. Epilepsia 46, 1780–1787 (2005).
  PubMed Google Scholar
• Forsgren, L. et al. Mortality of epilepsy in developed countries: a review. Epilepsia 46 (Suppl. 11), 18–27 (2005).
  PubMed Google Scholar
• Schapira, A. H. Present and future drug treatment for Parkinson's disease. J. Neurol. Neurosurg. Psychiatry 76, 1472–1478 (2005).
  CAS PubMed PubMed Central Google Scholar
• Lleo, A., Greenberg, S. M. & Growdon, J. H. Current pharmacotherapy for Alzheimer's disease. Annu. Rev. Med. 57, 513–533 (2006).
  CAS PubMed Google Scholar
• Gsell, W., Jungkunz, G. & Riederer, P. Functional neurochemistry of Alzheimer's disease. Curr. Pharm. Des. 10, 265–293 (2004).
  CAS PubMed Google Scholar
• Nance, M. A. & Myers, R. H. Juvenile onset Huntington's disease — clinical and research perspectives. Ment. Retard. Dev. Disabil. Res. Rev. 7, 153–157 (2001).
  CAS PubMed Google Scholar
• Weiner, M. F. et al. Can Alzheimer's disease and dementias with Lewy bodies be distinguished clinically? J. Geriatr. Psychiatry Neurol. 16, 245–250 (2003).
  PubMed Google Scholar
• Amatniek, J. C. et al. Incidence and predictors of seizures in patients with Alzheimer's disease. Epilepsia 47, 867–872 (2006).
  PubMed Google Scholar
• Mangiarini, L. et al. Exon 1 of the HD gene with an expanded CAG repeat is sufficient to cause a progressive neurological phenotype in transgenic mice. Cell 87, 493–506 (1996).
  CAS PubMed Google Scholar
• Del Vecchio, R. A., Gold, L. H., Novick, S. J., Wong, G. & Hyde, L. A. Increased seizure threshold and severity in young transgenic CRND8 mice. Neurosci. Lett. 367, 164–167 (2004).
  CAS PubMed Google Scholar
• Xie, C. W. Calcium-regulated signaling pathways: role in amyloid β-induced synaptic dysfunction. Neuromolecular Med. 6, 53–64 (2004).
  CAS PubMed Google Scholar
• Selkoe, D. J. & Schenk, D. Alzheimer's disease: molecular understanding predicts amyloid-based therapeutics. Annu. Rev. Pharmacol. Toxicol. 43, 545–584 (2003).
  CAS PubMed Google Scholar
• Grady, C. L. et al. Evidence from functional neuroimaging of a compensatory prefrontal network in Alzheimer's disease. J. Neurosci. 2, 986–993 (2003).
  Google Scholar
• Pariente, J. et al. Alzheimer's patients engage an alternative network during a memory task. Ann. Neurol. 58, 870–879 (2005).
  PubMed Google Scholar
• Nakanishi, S. Synaptic mechanisms of the cerebellar cortical network. Trends Neurosci. 28, 93–100 (2005).
  CAS PubMed Google Scholar
• Kobayashi, D. T. & Chen, K. S. Behavioral phenotypes of amyloid-based genetically modified mouse models of Alzheimer's Disease. Genes Brain Behav. 4, 173–196 (2005).
  CAS PubMed Google Scholar
• Janus, C. et al. Aβ peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease. Nature 408, 979–982 (2000).
  ADS CAS PubMed Google Scholar
• Morgan, D. et al. Aβ peptide vaccination prevents memory loss in an animal model of Alzheimer's disease. Nature 408, 982–985 (2000).
  ADS CAS PubMed Google Scholar
• Dodart, J. C. et al. Immunization reverses memory deficits without reducing brain Aβ burden in Alzheimer's disease model. Nature Neurosci. 5, 452–457 (2002).
  CAS PubMed Google Scholar
• Kotilinek, L. A. et al. Reversible memory loss in a mouse transgenic model of Alzheimer's disease. J. Neurosci. 22, 6331–6335 (2002).
  CAS PubMed PubMed Central Google Scholar
• Yamamoto, A., Lucas, J. J. & Hen, R. Reversal of neuropathology and motor dysfunction in a conditional model of Huntington's disease. Cell 101, 57–66 (2000).
  CAS PubMed Google Scholar
• Martin-Aparicio, E. et al. Proteasomal-dependent aggregate reversal and absence of cell death in a conditional mouse model of Huntington's disease. J. Neurosci. 21, 8772–8781 (2001).
  CAS PubMed PubMed Central Google Scholar
• Masliah, E. et al. Effects of α-synuclein immunization in a mouse model of Parkinson's disease. Neuron 46, 857–868 (2005).
  CAS PubMed Google Scholar
• Brandt, R., Hundelt, M. & Shahani, N. Tau alteration and neuronal degeneration in tauopathies: mechanisms and models. Biochim. Biophys. Acta 1739, 331–354 (2005).
  CAS PubMed Google Scholar
• Santacruz, K. et al. Tau suppression in a neurodegenerative mouse model improves memory function. Science 309, 476–481 (2005).
  ADS CAS PubMed PubMed Central Google Scholar
• Chin, J. et al. Fyn kinase induces synaptic and cognitive impairments in a transgenic mouse model of Alzheimer's disease. J. Neurosci. 25, 9694–9703 (2005).
  CAS PubMed PubMed Central Google Scholar
• Dickey, C. A. et al. Selectively reduced expression of synaptic plasticity-related genes in amyloid precursor protein + presenilin-1 transgenic mice. J. Neurosci. 23, 5219–5226 (2003).
  CAS PubMed PubMed Central Google Scholar
• Lacor, P. N. et al. Synaptic targeting by Alzheimer's-related amyloid β oligomers. J. Neurosci. 24, 10191–10200 (2004).
  CAS PubMed PubMed Central Google Scholar
• Cotman, C. W., Hailer, N. P., Pfister, K. K., Soltesz, I. & Schachner, M. Cell adhesion molecules in neural plasticity and pathology: similar mechanisms, distinct organizations? Prog. Neurobiol. 55, 659–669 (1998).
  CAS PubMed Google Scholar
• Wang, Q., Walsh, D. M., Rowan, M. J., Selkoe, D. J. & Anwyl, R. Block of long-term potentiation by naturally secreted and synthetic amyloid β-peptide in hippocampal slices is mediated via activation of the kinases c-Jun N-terminal kinase, cyclin-dependent kinase 5, and p38 mitogen-activated protein kinase as well as metabotropic glutamate receptor type 5. J. Neurosci. 24, 3370–3378 (2004).
  CAS PubMed PubMed Central Google Scholar
• Snyder, E. M. et al. Regulation of NMDA receptor trafficking by amyloid-β. Nature Neurosci. 8, 1051–1058 (2005).
  CAS PubMed Google Scholar
• Oddo, S. & LaFerla, F. M. The role of nicotinic acetylcholine receptors in Alzheimer's disease. J. Physiol. (Paris) 99, 172–179 (2006).
  CAS Google Scholar
• Kelly, B. L., Vassar, R. & Ferreira, A. β-amyloid-induced dynamin 1 depletion in hippocampal neurons. A potential mechanism for early cognitive decline in Alzheimer disease. J. Biol. Chem. 280, 31746–31753 (2005).
  CAS PubMed Google Scholar
• Haddad, J. J. Mitogen-activated protein kinases and the evolution of Alzheimer's: a revolutionary neurogenetic axis for therapeutic intervention? Prog. Neurobiol. 73, 359–377 (2004).
  CAS PubMed Google Scholar
• Lee, G. Tau and src family tyrosine kinases. Biochim. Biophys. Acta 1739, 323–330 (2005).
  CAS PubMed Google Scholar
• Giese, K. P., Ris, L. & Plattner, F. Is there a role of the cyclin-dependent kinase 5 activator p25 in Alzheimer's disease? Neuroreport 16, 1725–1730 (2005).
  CAS PubMed Google Scholar
• Roselli, F. et al. Soluble β-amyloid1–40 induces NMDA-dependent degradation of postsynaptic density-95 at glutamatergic synapses. J. Neurosci. 25, 11061–11070 (2005).
  CAS PubMed PubMed Central Google Scholar
• Almeida, C.G. et al. Beta-amyloid accumulation in APP mutant neurons reduces PSD-95 and GluR1 in synapses. Neurobiol. Dis. 20, 187–198 (2005).
  CAS PubMed Google Scholar
• Hsia, A. et al. Plaque-independent disruption of neural circuits in Alzheimer's disease mouse models. Proc. Natl Acad. Sci. USA 96, 3228–3233 (1999).
  ADS CAS PubMed PubMed Central Google Scholar
• Mucke, L. et al. High-level neuronal expression of Aβ1–42 in wild-type human amyloid protein precursor transgenic mice: synaptotoxicity without plaque formation. J. Neurosci. 20, 4050–4058 (2000).
  CAS PubMed PubMed Central Google Scholar
• Moolman, D. L., Vitolo, O. V., Vonsattel, J. P. & Shelanski, M. L. Dendrite and dendritic spine alterations in Alzheimer models. J. Neurocytol. 33, 377–387 (2004).
  CAS PubMed Google Scholar
• Kamenetz, F. et al. APP processing and synaptic function. Neuron 37, 925–937 (2003).
  CAS PubMed Google Scholar
• Chapman, P. F. et al. Impaired synaptic plasticity and learning in aged amyloid precursor protein transgenic mice. Nature Neurosci. 2, 271–276 (1999).
  CAS PubMed Google Scholar
• Walsh, D. M. et al. Naturally secreted oligomers of amyloid β protein potently inhibit hippocampal long-term potentiation in vivo. Nature 416, 535–539 (2002).
  ADS CAS PubMed Google Scholar