References
- Hachinski VC, Potter P, Merskey H. Leuko-araiosis: an ancient term for a new problem. Can. J. Neurol. Sci.13, 533–534 (1986).
- Steingart A, Hachinski VC, Lau C et al. Cognitive and neurologic findings in subjects with diffuse white matter lucencies on computed tomographic scan (leuko-araiosis). Arch. Neurol.44, 32–35 (1987).
- Steingart A, Hachinski VC, Lau C et al. Cognitive and neurologic findings in demented patients with diffuse white matter lucencies on computed tomographic scan (leuko-araiosis). Arch. Neurol.44, 36–39 (1987).
- Junque C, Pujol J, Vendrell P et al. Leuko-araiosis on magnetic resonance imaging and speed of mental processing. Arch. Neurol.47, 151–156 (1990).
- Liu CK, Miller BL, Cummings JL et al. A quantitative MRI study of vascular dementia. Neurology42, 138–143 (1992).
- Inzitari D, Simoni M, Pracucci G et al. Risk of rapid global functional decline in elderly patients with severe cerebral age-related white matter changes: the LADIS study. Arch. Intern. Med.167, 81–88 (2007).
- Ylikoski R, Ylikoski A, Erkinjuntti T et al. White matter changes in healthy elderly persons correlate with attention and speed of mental processing. Arch. Neurol.50, 818–824 (1993).
- Pantoni L, Garcia JH. Pathogenesis of leukoaraiosis, a review. Stroke28, 652–659 (1997).
- Pantoni L. Pathophysiology of age-related cerebral white matter changes. Cerebrovasc. Dis.13(Suppl. 2), 7–14 (2002).
- Pantoni L, Poggesi A, Basile AM et al. Leukoaraiosis predicts hidden global functioning impairment in nondisabled older people: the LADIS (Leukoaraiosis and Disability in the Elderly) Study. J. Am. Geriatr. Soc.54, 95–101 (2006).
- van Gijn J. Leukoaraiosis and vascular dementia. Neurology51, 3–8 (1998).
- Hassan A, Hunt BJ, O’Sullivan M et al. Markers of endothelial dysfunction in lacunar infarction and ischaemic leukoaraiosis. Brain126, 424–432 (2003).
- Wada M, Nagasawa H, Kurita K et al. Microalbuminuria is a risk factor for cerebral small vessel disease in community-based elderly subjects. J. Neurol. Sci.255, 27–34 (2007).
- Hoth KF, Tate DF, Poppas A et al. Endothelial function and white matter hyperintensities in older adults with cardiovascular disease. Stroke38, 308–312 (2007).
- Clarke R, Joachim C, Esiri M et al. Leukoaraiosis at presentation and disease progression during follow-up in histologically confirmed cases of dementia. Ann. NY Acad. Sci.903, 497–500 (2000).
- Wright CB, Paik MC, Brown TR et al. Total homocysteine is associated with white matter hyperintensity volume: the Northern Manhattan Study. Stroke36, 1207–1211 (2005).
- Pak KJ, Chan SL, Mattson MP. Homocysteine and folate deficiency sensitize oligodendrocytes to the cell death-promoting effects of a presenilin-1 mutation and amyloid beta-peptide. Neuromolecular Med.3, 119–128 (2003).
- Szolnoki Z. Chemical events behind leukoaraiosis: medicinal chemistry offers new insight into a specific microcirculation disturbance in the brain (a chemical approach to a frequent cerebral phenotype). Curr. Med. Chem.14, 1027–1036 (2007).
- Szolnoki Z. Pathomechanism of leukoaraiosis: a molecular bridge between the genetic, biochemical, and clinical processes (a mitochondrial hypothesis). Neuromolecular Med.9, 21–34 (2007).
- Brown WR, Moody DM, Thore CR et al. Vascular dementia in leukoaraiosis may be a consequence of capillary loss not only in the lesions, but in normal-appearing white matter and cortex as well. J. Neurol. Sci.257, 62–66 (2007).
- Yao H, Sadoshima S, Ibayashi S et al. Leukoaraiosis and dementia in hypertensive patients. Stroke23, 1673–1677 (1992).
- Amar K, Macgowan S, Wilcock G et al. Are genetic factors important in the aetiology of leukoaraiosis? Results from a memory clinic population. Int. J. Geriat. Psychiatry13, 585–590 (1998).
- Hassan A, Lansbury A, Catto AJ et al. Angiotensin converting enzyme insertion/deletion genotype is associated with leukoaraiosis in lacunar syndromes. J. Neurol. Neurosurg. Psychiatry72, 343–346 (2002).
- Sierra C, Coca A, Gómez-Angelats E et al. Renin–angiotensin system genetic polymorphisms and cerebral white matter lesions in essential hypertension. Hypertension39, 343–347 (2002).
- Szolnoki Z, Somogyvári F, Kondacs A et al. Evaluation of the roles of common genetic mutations in leukoaraiosis. Acta Neurol. Scand.104, 281–287 (2001).
- Tian J, Shi J, Bailey K et al. A polymorphism in the angiotensin 1-converting enzyme gene is associated with damage to cerebral cortical white matter in Alzheimer’s disease. Neurosci. Lett.354, 103–106 (2004).
- De Ciuceis C, Amiri F, Brassard P et al. Reduced vascular remodeling, endothelial dysfunction, and oxidative stress in resistance arteries of angiotensin II-infused macrophage colony-stimulating factor-deficient mice: evidence for a role in inflammation in angiotensin-induced vascular injury. Arterioscler. Thromb. Vasc. Biol.25, 2106–2113 (2005).
- Watanabe S, Tagawa T, Yamakawa K et al. Inhibition of the renin–angiotensin system prevents free fatty acid-induced acute endothelial dysfunction in humans. Arterioscler. Thromb. Vasc. Biol.25, 2376–2380 (2005).
- Ginanneschi A, Marinoni M, Inzitari D et al. Blood pressure monitoring in patients with leukoaraiosis. Neurology42(Suppl. 3), 273 (1992).
- Harrison MJ, Marshall J. Hypoperfusion in the aetiology of subcortical arteriosclerotic encephalopathy (Binswanger type). J. Neurol. Neurosurg. Psychiatry47, 754 (1984).
- Matsushita K, Kuriyama Y, Nagatsuka K. Periventricular white matter lucency and cerebral blood flow autoregulation in hypertensive patients. Hypertension23, 565–568 (1994).
- McQuinn BA, O’Leary DH. White matter lucencies on computed tomography, subacute arteriosclerotic encephalopathy (Binswanger’s disease), and blood pressure. Stroke18, 900–905 (1987).
- Shimada K, Kawamoto A, Matsubayashi K et al. Diurnal blood pressure variations and silent cerebrovascular damage in elderly patients with hypertension. J. Hypertens.10, 875–878 (1992).
- Schmidt H, Fazekas F, Kostner GM et al. Angiotensinogen gene promoter haplotype and microangiopathy-related cerebral damage: results of the Austrian Stroke Prevention Study. Stroke32, 405–412 (2001).
- Sachdev P, Parslow R, Salonikas C et al. Homocysteine and the brain in midadult life: evidence for an increased risk of leukoaraiosis in men. Arch. Neurol.61, 1369–1376 (2004).
- Welch GN, Loscalzo J. Homocysteine and atherothrombosis. N. Engl. J. Med.338, 1042–1050 (1998).
- Wen HM, Baum L, Cheung WS et al. Apolipoprotein E epsilon4 allele is associated with the volume of white matter changes in patients with lacunar infarcts. Eur. J. Neurol.13, 1216–1220 (2006).
- Persson J, Lind J, Larsson A et al. Altered brain white matter integrity in healthy carriers of the APOE epsilon4 allele: a risk for AD? Neurology66, 1029–1033 (2006).
- Lemmens R, Görner A, Schrooten M, Thijs V. Association of apolipoprotein E epsilon2 with white matter disease but not with microbleeds. Stroke38, 1185–1188 (2007).
- Bartzokis G, Lu PH, Geschwind DH et al. Apolipoprotein E affects both myelin breakdown and cognition: implications for age-related trajectories of decline into dementia. Biol. Psychiatry62(12), 1380–1387 (2007).
- Høgh P, Garde E, Mortensen EL et al. The apolipoprotein E epsilon4-allele and antihypertensive treatment are associated with increased risk of cerebral MRI white matter hyperintensities. Acta. Neurol. Scand.115, 248–253 (2007).
- Szolnoki Z, Somogyvári F, Kondacs A et al. Specific APO E genotypes in combination with the ACE D/D or MTHFR 677TT mutation yield an independent genetic risk of leukoaraiosis. Acta. Neurol. Scand.109, 222–227 (2004).
- Schmidt R, Schmidt H, Fazekas F et al. MRI cerebral white matter lesions and paraoxonase PON1 polymorphism: three-year follow-up of the Austrian Stroke Prevention Study. Arterioscler. Thromb. Vasc. Biol.20, 1811–1816 (2000).
- Fornage M, Mosley TH, Jack CR et al. Family-based association study of matrix metalloproteinase-3 and -9 haplotypes with susceptibility to ischemic white matter injury. Hum. Genet.120, 671–680 (2007).
- Szolnoki Z, Kondacs A, Mandi Y, Somogyvari F. A genetic variant in cytoskeleton motors amplifies susceptibility to leukoaraiosis in hypertensive smokers: gene–environmental interactions behind vascular white matter demyelinization. J. Mol. Neurosci.33, 173–179 (2007).
- Szolnoki Z. Genetic variant-associated endothelial dysfunction behind small-vessel cerebral circulatory disorders: a new pathomechanism behind common cerebral phenotypes. Mini Rev. Med. Chem.7, 527–530 (2007).
- Szolnoki Z. A dynamically changing intracellular water network serves as a universal regulator of the cell: the water-governed cycle. Biochem. Biophys. Res. Commun.357, 331–334 (2007).
- Csordas A, Mazlo M, Gallyas F. Recovery versus death of “dark” (compacted) neurons in a nonimpaired parenchymal environment: light and electron microscopic observation. Acta Neuropathol. (Berl.)106, 37–49 (2003).
- Gallyas F, Farkas O, Mazlo M. Gel-to-gel phase transition may occur in mammalian cells: mechanism of formation of “dark” (compacted) neurons. Biol. Cell.96, 313–324 (2004).
- Gallyas F, Gasz B, Szigeti A, Mazlo M. Pathological circumstances impair the ability of “dark” neurons to undergo spontaneous recovery. Brain Res.1110, 211–220 (2006).
- Zsombok A, Toth Z, Gallyas F. Basophilia, acidophilia and argyrophilia of “dark” (compacted) neurons during their formation, recovery or death in an otherwise undamaged environment. J. Neurosci. Methods142, 145–152 (2005).
- Csermely P. Strong links are important but weak links stabilize them. Trends Biochem. Sci.29, 331–334 (2004).
- Otzen DE, Oliveberg M. Salt-induced detour through compact regions of the protein folding landscape. Proc. Natl Acad. Sci. USA96, 11746–11751 (1999).
- Csermely P. Water and cellular folding processes. Cell. Mol. Biol.47, 797–800 (2001).
- Doye JP. The network topology of a potential energy landscape: a static scale-free network. Phys. Rev. Lett.88, 238701 (2002).
- Plotkin SS, Wolynes PG. Buffered energy landscapes: another solution to the kinetic paradoxes of protein folding. Proc. Natl Acad. Sci. USA100, 4417–4422 (2003).
- Barron LD, Hecht L, Wilson G. The lubricant life: a proposal that solvent water promotes extremely fast conformational fluctuations in mobile heteropolypeptide structure. Biochemistry36, 13143–13147 (1997).
- Levy Y, Onuchic JN. Water and proteins: a love–hate relationship. Proc. Natl Acad. Sci. USA101, 3325–3326 (2004).
- Papoian GA, Ulander J, Eastwood MP et al. Water in protein structure prediction. Proc. Natl Acad. Sci. USA101, 3352–3357 (2004).
- Rao F, Caflisch A. The protein folding network. J. Mol. Biol.342, 299–306 (2004).
- Klibanov AM. What is remembered and why? Nature374(6523), 596 (1995).
- Lehninger AL. Glycolysis. In: Biochemistry. Lehninger AL (Ed.). Worth Publisher Inc., NY, USA 417–443 (1975).
- Lehninger AL. Oxidative phosphorylation, mitochondrial structure and the compartmentation of respiratory metabolism. In: Biochemistry. Lehninger AL (Ed.). Worth Publisher Inc., NY, USA 509–542 (1975).
- Ravasz E, Somera AL, Mongru DA et al. Hierarchical organization of modularity in metabolic network. Science297, 1551–1555 (2002).
- Feynman RP, Leighton RB, Sands M. Section 21.9. In: The Feynman Lectures on Physics. Volume 3. Quantum Mechanics. Addison-Wesley Professional, Boston, MA, USA (1965).
- Winfree AT. Biological rhythms and behaviour of populations of coupled oscillators J. Theor. Biol.16, 15–42 (1967).
- Lindner JF. Meadows BK, Ditto WL. Array enhanced stochastic resonance and spatiotemporal synchronization. Phys. Rev. Lett.75, 3–6 (1995).
- Bressloff PC, Coombes S. Travelling waves in a chain of pulse-coupled oscillators. Phys. Rev. Lett.80, 4815–4818 (1998).
- Blasius B, Huppert A, Stone L. Complex dynamics and phase synchronization in spatially extended ecological systems. Nature399, 354–359 (1999).
- Gao Z, Hu B, Hu G. Stochastic resonance of small-world networks. Phys. Rev.E65, 016209 (2001).
- Ponzi A, Aizawa Y. Criticality and punctuated equilibrium in a spin system model of a financial market. Chaos Solution Fractals11, 1739–1746 (2002).
- Derenyi I, Farkas I, Palla G, Vicsek T. Topological phase transitions of random networks. Physica A334, 583–590 (2004).
- Palla G, Derenyi I, Farkas I, Vicsek T. Statistical mechanics of topological phase transitions in networks. Phys. Rev.E69, 046117 (2004).
- Jeong H, Mason SP, Barabasi AL, Oltvai ZN. Lethality and centrality in protein networks. Nature411, 41–42 (2001).
- Soti C, Sreedhar AS, Csermely P. Apoptosis, necrosis and cellular senescence: chaperone occupancy as a potential switch. Aging Cell2, 39–45 (2003).
- Kenworthy AK, Nichols BJ, Remmert CL et al. Dymamics of putative raft-associated proteins at the cell surface. J. Cell. Biol.165, 735–746 (2004).
- Abe K, Aoki M, Kawagoe J et al. Ischemic delayed neuronal death. A mitochondrial hypothesis. Stroke26, 1478–1489 (1995).
- Gallyas F, Zoltay G, Dames W. Formation of “dark” (argyrophilic) neurons of various origins proceeds with a common mechanism of biophysical nature (a novel hypothesis). Acta Neuropathol. (Berl.)83, 4–9 (1992).
- Gallyas F, Zoltay G, Horvath Z et al. An immediate morphopathologic response of neurons to electroshock; a reliable model for producing “dark” neurons in experimental neuropathology. Neurobiology (Bp.)1, 133–146 (1993).
- Sawada H, Udaka F, Izumi Y et al. Cerebral white matter lesions are not associated with ApoE genotype but with age and female sex in Alzheimer’s disease. J. Neurol. Neurosurg. Psychiatry68, 653–666 (2000).
- Schmidt R, Schmidt H, Fazekas F et al. Apolipoprotein E polymorphism and silent microangiopathy-related cerebral damage. Results of the Austrian Stroke Prevention Study. Stroke28, 951–956 (1997).