Isidre Ferrer



  1. Dominguez Gonzalez M, Puigpinós M, Jove M, Naudi A, Portero Otin M, Pamplona R, et al. Regional vulnerability to lipoxidative damage and inflammation in normal human brain aging. Exp Gerontol. 2018;111:218-228 pubmed publisher
    ..However, no clear relationship can be established between NKT, MDA, COX-2 and CYP2J2 levels, and regional vulnerability to neurodegeneration in old age. ..
  2. Ferrer I. Oligodendrogliopathy in neurodegenerative diseases with abnormal protein aggregates: The forgotten partner. Prog Neurobiol. 2018;169:24-54 pubmed publisher
  3. Ferrer I, Olive M. Molecular pathology of myofibrillar myopathies. Expert Rev Mol Med. 2008;10:e25 pubmed publisher
  4. Ferrer I, Martinez A, Blanco R, Dalfó E, Carmona M. Neuropathology of sporadic Parkinson disease before the appearance of parkinsonism: preclinical Parkinson disease. J Neural Transm (Vienna). 2011;118:821-39 pubmed publisher
  5. Del Río J, Ferrer I, Gavin R. Role of cellular prion protein in interneuronal amyloid transmission. Prog Neurobiol. 2018;165-167:87-102 pubmed publisher
    ..This review summarizes current knowledge about PrPC as a putative receptor for amyloid proteins and the physiological consequences of these interactions. ..
  6. Ferrer I. Selection of controls in the study of human neurodegenerative diseases in old age. J Neural Transm (Vienna). 2015;122:941-7 pubmed publisher
    ..The absence of neurological and mental symptoms and signs, although a sine qua non condition, is not sufficient to match control and problem cases for research. ..
  7. Ansoleaga B, Garcia Esparcia P, Pinacho R, Haro J, Ramos B, Ferrer I. Decrease in olfactory and taste receptor expression in the dorsolateral prefrontal cortex in chronic schizophrenia. J Psychiatr Res. 2015;60:109-16 pubmed publisher
    ..In addition, the influence of antipsychotics on the expression of ORs and TASRs in schizophrenia suggests that these receptors could be involved in the mechanism of action or side effects of antipsychotics. ..
  8. Ferrer I. Defining Alzheimer as a common age-related neurodegenerative process not inevitably leading to dementia. Prog Neurobiol. 2012;97:38-51 pubmed publisher
    ..In this context, the first stages of Alzheimer should be considered as primary targets of therapeutic intervention in order to prevent progression to diseased states. ..
  9. Cabre R, Naudi A, Dominguez Gonzalez M, Ayala V, Jove M, Mota Martorell N, et al. Sixty years old is the breakpoint of human frontal cortex aging. Free Radic Biol Med. 2017;103:14-22 pubmed publisher

More Information


  1. request reprint
    Ansoleaga B, Garcia Esparcia P, Llorens F, Hernández Ortega K, Carmona Tech M, Antonio Del Río J, et al. Altered Mitochondria, Protein Synthesis Machinery, and Purine Metabolism Are Molecular Contributors to the Pathogenesis of Creutzfeldt-Jakob Disease. J Neuropathol Exp Neurol. 2016;: pubmed
    ..These findings point to altered mRNA and protein expression of components of mitochondria, protein synthesis machinery, and purine metabolism as components of the pathogenesis of CJD. ..
  2. López González I, Garcia Esparcia P, Llorens F, Ferrer I. Genetic and Transcriptomic Profiles of Inflammation in Neurodegenerative Diseases: Alzheimer, Parkinson, Creutzfeldt-Jakob and Tauopathies. Int J Mol Sci. 2016;17:206 pubmed publisher
  3. Domínguez M, de Oliveira E, Odena M, Portero M, Pamplona R, Ferrer I. Redox proteomic profiling of neuroketal-adducted proteins in human brain: Regional vulnerability at middle age increases in the elderly. Free Radic Biol Med. 2016;95:1-15 pubmed publisher
    ..Oligomers significantly correlated with NKT levels in the three cortical regions, suggesting that protein NKT adduction parallels soluble oligomer formation. ..
  4. Ferrer I. Proteomics and lipidomics in the human brain. Handb Clin Neurol. 2018;150:285-302 pubmed publisher
    ..Information about certain altered protein clusters and proteins oxidatively damaged is summarized for Alzheimer and Parkinson diseases. ..
  5. Naudi A, Cabre R, Dominguez Gonzalez M, Ayala V, Jove M, Mota Martorell N, et al. Region-specific vulnerability to lipid peroxidation and evidence of neuronal mechanisms for polyunsaturated fatty acid biosynthesis in the healthy adult human central nervous system. Biochim Biophys Acta Mol Cell Biol Lipids. 2017;1862:485-495 pubmed publisher
    ..In conclusion, our results suggest that there is a region-specific vulnerability to lipid peroxidation and offer evidence of neuronal mechanisms for polyunsaturated fatty acid biosynthesis in the human central nervous system. ..
  6. Lopez Gonzalez I, Viana R, Sanz P, Ferrer I. Inflammation in Lafora Disease: Evolution with Disease Progression in Laforin and Malin Knock-out Mouse Models. Mol Neurobiol. 2017;54:3119-3130 pubmed publisher
    ..These findings also point to the possibility of using anti-inflammatory agents to mitigate the degenerative process in LD. ..
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    Llorens F, Thune K, Schmitz M, Ansoleaga B, Frau Méndez M, Cramm M, et al. Identification of new molecular alterations in fatal familial insomnia. Hum Mol Genet. 2016;25:2417-2436 pubmed
  8. Cacabelos D, Ramírez Núñez O, Granado Serrano A, Torres P, Ayala V, Moiseeva V, et al. Early and gender-specific differences in spinal cord mitochondrial function and oxidative stress markers in a mouse model of ALS. Acta Neuropathol Commun. 2016;4:3 pubmed publisher
    ..This study is important in the effort to further understanding of whether different degrees of spinal cord mitochondrial dysfunction could be disease modifiers in ALS. ..
  9. Garcia Esparcia P, Hernández Ortega K, Koneti A, Gil L, Delgado Morales R, Castaño E, et al. Altered machinery of protein synthesis is region- and stage-dependent and is associated with α-synuclein oligomers in Parkinson's disease. Acta Neuropathol Commun. 2015;3:76 pubmed publisher
  10. Llorens F, Zarranz J, Fischer A, Zerr I, Ferrer I. Fatal Familial Insomnia: Clinical Aspects and Molecular Alterations. Curr Neurol Neurosci Rep. 2017;17:30 pubmed publisher
    ..Although the development of a therapy is still a major challenge, recent findings represent a step toward understanding of the clinical and molecular aspects of FFI. ..
  11. Llorens F, Thune K, Andrés Benito P, Tahir W, Ansoleaga B, Hernández Ortega K, et al. MicroRNA Expression in the Locus Coeruleus, Entorhinal Cortex, and Hippocampus at Early and Middle Stages of Braak Neurofibrillary Tangle Pathology. J Mol Neurosci. 2017;63:206-215 pubmed publisher
  12. Ferrer I, Vidal N. Neuropathology of cerebrovascular diseases. Handb Clin Neurol. 2017;145:79-114 pubmed publisher
    ..Cognitive impairment of vascular origin deserves an individual section. ..
  13. Ansoleaga B, Jové M, Schlüter A, Garcia Esparcia P, Moreno J, Pujol A, et al. Deregulation of purine metabolism in Alzheimer's disease. Neurobiol Aging. 2015;36:68-80 pubmed publisher
    ..Our results indicate stage- and region-dependent deregulation of purine metabolism in AD. ..
  14. Ferrer I, Aubourg P, Pujol A. General aspects and neuropathology of X-linked adrenoleukodystrophy. Brain Pathol. 2010;20:817-30 pubmed publisher
  15. Ferrer I. Altered mitochondria, energy metabolism, voltage-dependent anion channel, and lipid rafts converge to exhaust neurons in Alzheimer's disease. J Bioenerg Biomembr. 2009;41:425-31 pubmed publisher
    ..Cell exhaustion is suggested as being a determining element to interpret impaired neuron function, reduced molecular turnover, and enhanced cell death. ..
  16. Cacabelos D, Ayala V, Granado Serrano A, Jové M, Torres P, Boada J, et al. Interplay between TDP-43 and docosahexaenoic acid-related processes in amyotrophic lateral sclerosis. Neurobiol Dis. 2016;88:148-60 pubmed publisher
    ..Later on, this allostatic overload could exacerbate cell stress by contributing to TDP-43 aggregation. This, at its turn, could blunt this protective response, overall leading to DHA depletion and neuronal dysfunction. ..
  17. Ansoleaga B, Garcia Esparcia P, Llorens F, Moreno J, Aso E, Ferrer I. Dysregulation of brain olfactory and taste receptors in AD, PSP and CJD, and AD-related model. Neuroscience. 2013;248:369-82 pubmed publisher