Brain banks as key part of biochemical and molecular studies on cerebral cortex involvement in Parkinson’s disease

Exciting developments in basic and clinical neuroscience and recent progress in the field of Parkinson’s disease (PD) are partly a result of the availability of human specimens obtained through brain banks. These banks have optimized the methodological, managerial and organizational procedures; standard operating procedures; and ethical, legal and social issues, including the code of conduct for 21st Century brain banking and novel protocols. The present minireview focuses on current brain banking organization and management, as well as the likely future direction of the brain banking field. We emphasize the potentials and pitfalls when using high‐quality specimens of the human central nervous system for advancing PD research. PD is a generalized disease in which α‐synuclein is not a unique component but, instead, is only one of the players accounting for the complex impairment of biochemical/molecular processes involved in metabolic pathways. This is particularly important in the cerebral cortex, where altered cognition has a complex neurochemical substrate. Mitochondria and energy metabolism impairment, abnormal RNA, microRNA, protein synthesis, post‐translational protein modifications and alterations in the lipid composition of membranes and lipid rafts are part of these complementary factors. We have to be alert to the possible pitfalls of each specimen and its suitability for a particular study. Not all samples qualify for the study of DNA, RNA, proteins, post‐translational modifications, lipids and metabolomes, although the use of carefully selected samples and appropriate methods minimizes pitfalls and errors and guarantees high‐quality reserach.

[1]  P. Riederer,et al.  Comparison analysis of gene expression patterns between sporadic Alzheimer's and Parkinson's disease. , 2007, Journal of Alzheimer's disease : JAD.

[2]  M. Portero-Otín,et al.  Protein Targets of Oxidative Damage in Human Neurodegenerative Diseases with Abnormal Protein Aggregates , 2010, Brain pathology.

[3]  W. Schulz-Schaeffer The synaptic pathology of α-synuclein aggregation in dementia with Lewy bodies, Parkinson’s disease and Parkinson’s disease dementia , 2010, Acta Neuropathologica.

[4]  Yoav Ben-Shlomo,et al.  The accuracy of diagnosis of parkinsonian syndromes in a specialist movement disorder service. , 2002, Brain : a journal of neurology.

[5]  R. Ravid Biobanks for biomarkers in neurological disorders The Da Vinci bridge for optimal clinico-pathological connection , 2009, Journal of the Neurological Sciences.

[6]  H. Braak,et al.  Staging of brain pathology related to sporadic Parkinson’s disease , 2003, Neurobiology of Aging.

[7]  G. Muntané,et al.  Phosphorylation of tau and α-synuclein in synaptic-enriched fractions of the frontal cortex in Alzheimer’s disease, and in Parkinson’s disease and related α-synucleinopathies , 2008, Neuroscience.

[8]  R. Ravid,et al.  Controls are what makes a brain bank go round , 1995 .

[9]  Isidre Ferrer,et al.  Evidence of Oxidative Stress in the Neocortex in Incidental Lewy Body Disease , 2005, Journal of neuropathology and experimental neurology.

[10]  Winnie S. Liang,et al.  Neuronal gene expression correlates of Parkinson's disease with dementia , 2008, Movement disorders : official journal of the Movement Disorder Society.

[11]  Hans Kretzschmar,et al.  Brain banking: opportunities, challenges and meaning for the future , 2009, Nature Reviews Neuroscience.

[12]  R. Albin,et al.  Cerebral Glucose Metabolic Features of Parkinson Disease and Incident Dementia: Longitudinal Study , 2011, The Journal of Nuclear Medicine.

[13]  M. Barrachina,et al.  Abnormal alpha-synuclein interactions with rab3a and rabphilin in diffuse Lewy body disease. , 2004, Neurobiology of disease.

[14]  R. Ravid Standard Operating Procedures, ethical and legal regulations in BTB (Brain/Tissue/Bio) banking: what is still missing? , 2008, Cell and Tissue Banking.

[15]  Allan I. Levey,et al.  Oxidative Modifications and Down-regulation of Ubiquitin Carboxyl-terminal Hydrolase L1 Associated with Idiopathic Parkinson's and Alzheimer's Diseases* , 2004, Journal of Biological Chemistry.

[16]  D. Dickson,et al.  Neuropathology of non-motor features of Parkinson disease. , 2009, Parkinsonism & related disorders.

[17]  C. Hulette Brain Banking in the United States , 2003, Journal of neuropathology and experimental neurology.

[18]  I. Ferrer,et al.  Human brain cortex: mitochondrial oxidative damage and adaptive response in Parkinson disease and in dementia with Lewy bodies. , 2009, Free radical biology & medicine.

[19]  J. Vonsattel,et al.  Twenty-first century brain banking. Processing brains for research: the Columbia University methods , 2007, Acta Neuropathologica.

[20]  Hui Yang,et al.  Mitochondrial dysfunction induced by knockdown of mortalin is rescued by Parkin. , 2011, Biochemical and biophysical research communications.

[21]  Houeto Jean-Luc [Parkinson's disease]. , 2022, La Revue du praticien.

[22]  David S. Park,et al.  Animal Models of Parkinson's Disease , 2011, Parkinson's disease.

[23]  Mauro Fasano,et al.  Cellular models to investigate biochemical pathways in Parkinson’s disease , 2012, The FEBS journal.

[24]  Xavier Estivill,et al.  MicroRNA profiling of Parkinson's disease brains identifies early downregulation of miR-34b/c which modulate mitochondrial function. , 2011, Human molecular genetics.

[25]  A. Levey,et al.  Oxidative Modifications and Aggregation of Cu,Zn-Superoxide Dismutase Associated with Alzheimer and Parkinson Diseases* , 2005, Journal of Biological Chemistry.

[26]  G. Santpere,et al.  Severe Alterations in Lipid Composition of Frontal Cortex Lipid Rafts from Parkinson’s Disease and Incidental Parkinson’s Disease , 2011, Molecular medicine.

[27]  Min Shi,et al.  Biomarker discovery in neurodegenerative diseases: A proteomic approach , 2009, Neurobiology of Disease.

[28]  A. Kakita,et al.  Proteinase K-resistant α-synuclein is deposited in presynapses in human Lewy body disease and A53T α-synuclein transgenic mice , 2010, Acta Neuropathologica.

[29]  Isidre Ferrer,et al.  Early involvement of the cerebral cortex in Parkinson's disease: Convergence of multiple metabolic defects , 2009, Progress in Neurobiology.

[30]  Joon-Kee Yoon,et al.  A comparison of cerebral glucose metabolism in Parkinson's disease, Parkinson's disease dementia and dementia with Lewy bodies , 2007, European journal of neurology.

[31]  D. Dickson,et al.  Alpha-synuclein and the Lewy body disorders. , 2001, Current opinion in neurology.

[32]  M. Barrachina,et al.  Brain banks: benefits, limitations and cautions concerning the use of post-mortem brain tissue for molecular studies , 2008, Cell and Tissue Banking.

[33]  Constantinos Kallis,et al.  Lewy- and Alzheimer-type pathologies in Parkinson's disease dementia: which is more important? , 2011, Brain : a journal of neurology.

[34]  I. Ferrer,et al.  Assessing quantitative post‐mortem changes in the gray matter of the human frontal cortex proteome by 2‐D DIGE , 2008, Proteomics.

[35]  V. Dhawan,et al.  Metabolic abnormalities associated with mild cognitive impairment in Parkinson disease , 2008, Neurology.

[36]  I. Alafuzoff,et al.  α‐Synuclein pathology does not predict extrapyramidal symptoms or dementia , 2005, Annals of neurology.

[37]  이필휴 A comparison of cerebral glucose metabolism in Parkinson's disease, Parkinson's disease dementia and dementia with Lewy bodies , 2007 .

[38]  D. Dickson,et al.  Neurodegeneration: The Molecular Pathology of Dementia and Movement Disorders: Dickson/Neurodegeneration: The Molecular Pathology of Dementia and Movement Disorders , 2011 .

[39]  A. Wallin,et al.  Posterior cortical brain dysfunction in cognitively impaired patients with Parkinson’s disease – a rCBF scintigraphy study , 2007, Acta neurologica Scandinavica.

[40]  V. Dhawan,et al.  Changes in network activity with the progression of Parkinson's disease. , 2007, Brain : a journal of neurology.

[41]  Sheng Pan,et al.  Using ‘omics’ to define pathogenesis and biomarkers of Parkinson’s disease , 2010, Expert review of neurotherapeutics.

[42]  Anette Schrag,et al.  What are the most important nonmotor symptoms in patients with Parkinson's disease and are we missing them? , 2010, Movement disorders : official journal of the Movement Disorder Society.

[43]  M. Cameron Sullards,et al.  Oxidative Damage of DJ-1 Is Linked to Sporadic Parkinson and Alzheimer Diseases* , 2006, Journal of Biological Chemistry.

[44]  R. Ravid,et al.  Brain banking and the human hypothalamus--factors to match for, pitfalls and potentials. , 1992, Progress in brain research.

[45]  I. Ferrer,et al.  Neuropathology of sporadic Parkinson disease before the appearance of parkinsonism: preclinical Parkinson disease , 2011, Journal of Neural Transmission.

[46]  M. Barrachina,et al.  Abnormal α-synuclein interactions with rab3a and rabphilin in diffuse Lewy body disease , 2004, Neurobiology of Disease.

[47]  E. Dalfo,et al.  Early α-synuclein lipoxidation in neocortex in Lewy body diseases , 2008, Neurobiology of Aging.

[48]  I. Ferrer,et al.  Increased oxidation of certain glycolysis and energy metabolism enzymes in the frontal cortex in Lewy body diseases , 2009, Journal of neuroscience research.

[49]  Yan Wang,et al.  Mortalin: A Protein Associated With Progression of Parkinson Disease? , 2008, Journal of neuropathology and experimental neurology.