<clinical_study>
  <!-- This xml conforms to an XML Schema at:
    https://clinicaltrials.gov/ct2/html/images/info/public.xsd -->
  <required_header>
    <download_date>ClinicalTrials.gov processed this data on September 20, 2023</download_date>
    <link_text>Link to the current ClinicalTrials.gov record.</link_text>
    <url>https://clinicaltrials.gov/ct2/show/NCT01707719</url>
  </required_header>
  <id_info>
    <org_study_id>ERASE</org_study_id>
    <nct_id>NCT01707719</nct_id>
  </id_info>
  <brief_title>Isolated Erythrocyte Membrane Susceptibility to Photo-oxidative Stress in Alzheimer's Disease</brief_title>
  <official_title>Isolated Erythrocyte Membrane Susceptibility to Photo-oxidative Stress in Patients Affected by Alzheimer's Disease and Healthy Controls</official_title>
  <sponsors>
    <lead_sponsor>
      <agency>Raffaele Antonelli Incalzi</agency>
      <agency_class>Other</agency_class>
    </lead_sponsor>
  </sponsors>
  <source>Campus Bio-Medico University</source>
  <oversight_info>
    <has_dmc>Yes</has_dmc>
  </oversight_info>
  <brief_summary>
    <textblock>
      High lipid peroxidation and altered antioxidant defenses have been frequently reported in&#xD;
      Alzheimer's disease patients.&#xD;
&#xD;
      The purpose of this study is to investigate susceptibility to photo-oxidation of isolated&#xD;
      erythrocyte membranes, in patients affected by Alzheimer's disease and age- and sex-matched,&#xD;
      non demented subjects.&#xD;
    </textblock>
  </brief_summary>
  <detailed_description>
    <textblock>
      The study hypothesis is that high lipid peroxidation and decreased antioxidant defenses&#xD;
      characterize the natural history of Alzheimer's disease.&#xD;
&#xD;
      It will be evaluated the release of malondialdehyde (MDA) from ex-vivo photo-oxidized&#xD;
      erythrocyte ghosts, through a very easy and convenient lab procedure for the preparation of&#xD;
      erythrocyte membrane samples.&#xD;
&#xD;
      Isolated and purified red blood cell membranes will be in vitro exposed to oxidative stress&#xD;
      by UV-B radiation. The extent of cell membrane damage will be quantified by the fluorometric&#xD;
      determination of MDA.&#xD;
&#xD;
      Induction of oxidative stress through ultraviolet rays, unlike that obtained by chemical&#xD;
      oxidizing agents, is fully controllable, since it produces effects only during irradiation.&#xD;
      Moreover, using isolated erythrocyte membranes allows for a greater specificity in the&#xD;
      evaluation of MDA produced, and reduces the amount of blood required for the assay.&#xD;
&#xD;
      A portion of the blood sample (500 µL) will be sent to the laboratory of Lipinutragen&#xD;
      (spin-off of CNR- National Research Center Bologna, Italy) where an erythrocyte membrane&#xD;
      lipidomic analysis will be performed for the characterization of membrane phospholipids, in&#xD;
      order to determinate the different lipid components (saturated fatty acids, monounsaturated&#xD;
      and polyunsaturated, trans fatty acids), each one characterized by a different oxidative&#xD;
      reactivity.&#xD;
&#xD;
      Recently published papers showed a striking association between urinary excretion of cortisol&#xD;
      and the increase of some markers of oxidative damage of DNA and RNA (in humans). This finding&#xD;
      provides further support to the idea that chronic psychological stress, who is associated to&#xD;
      hypercortisolemia, can lead to an acceleration of the aging process.&#xD;
&#xD;
      The brain is a major target of the effects of glucocorticoids (CCS). The harmful consequences&#xD;
      of cortisol on the hippocampus (one of the first brain areas affected by Alzheimer's disease)&#xD;
      are well known. Some studies showed inverse correlations between cortisol levels and&#xD;
      neuropsychological performance in patients with depression, dementia as well as in people&#xD;
      treated chronically with CCS.&#xD;
&#xD;
      Alzheimer's disease is associated with states of hypercortisolism. Nonetheless, so far, its&#xD;
      correlation with the level of oxidative stress has not been studied. We will investigate the&#xD;
      relationship between 24h excretion of urinary cortisol and the level of malondialdehyde,&#xD;
      produced by isolated and purified red blood cell membranes, in vitro exposed to oxidative&#xD;
      stress by UV-B radiation.&#xD;
    </textblock>
  </detailed_description>
  <overall_status>Completed</overall_status>
  <start_date>June 2015</start_date>
  <completion_date type="Actual">November 2018</completion_date>
  <primary_completion_date type="Actual">November 2018</primary_completion_date>
  <study_type>Observational</study_type>
  <has_expanded_access>No</has_expanded_access>
  <study_design_info>
    <observational_model>Case-Control</observational_model>
    <time_perspective>Cross-Sectional</time_perspective>
  </study_design_info>
  <primary_outcome>
    <measure>Malondialdehyde assay</measure>
    <time_frame>At the time of recruitment</time_frame>
    <description>Isolated and purified red blood cell membranes will be in vitro exposed to oxidative stress by UV-B radiation. The extent of cell membrane damage will be quantified by the fluorometric determination of malondialdehyde.</description>
  </primary_outcome>
  <secondary_outcome>
    <measure>Relationship between urinary excretion of cortisol and levels of malondialdehyde</measure>
    <time_frame>At the time of recruitment</time_frame>
    <description>Hyperactivity of the hypothalamic pituitary adrenal axis has been frequently described in Alzheimer's disease. Recently published work reported an association between high secretion of cortisol and oxidative stress. We will investigate the relationship between 24 h excretion of urinary cortisol and the level of malondialdehyde, produced by isolated and purified red blood cell membranes, in vitro exposed to oxidative stress by UV-B radiation.</description>
  </secondary_outcome>
  <number_of_groups>2</number_of_groups>
  <enrollment type="Actual">48</enrollment>
  <condition>Alzheimer Disease</condition>
  <condition>Oxidative Stress</condition>
  <condition>Adrenocortical Hyperfunction</condition>
  <arm_group>
    <arm_group_label>Alzheimer's disease</arm_group_label>
  </arm_group>
  <arm_group>
    <arm_group_label>Non demented subjects</arm_group_label>
  </arm_group>
  <biospec_retention>Samples With DNA</biospec_retention>
  <biospec_descr>
    <textblock>
      Whole blood&#xD;
    </textblock>
  </biospec_descr>
  <eligibility>
    <study_pop>
      <textblock>
        Patients meeting NINCDS-ADRDA criteria for Alzheimer's disease and age- / sex-matched&#xD;
        elderly subjects without dementia, will be recruited from those referring neurologists or&#xD;
        geriatricians on an outpatient basis&#xD;
      </textblock>
    </study_pop>
    <sampling_method>Probability Sample</sampling_method>
    <criteria>
      <textblock>
        Inclusion Criteria:&#xD;
&#xD;
          -  Outpatients of both sexes diagnosed with Alzheimer's disease according to NINCDS-ADRDA&#xD;
             criteria.&#xD;
&#xD;
          -  Age and sex-matched elderly subjects without dementia.&#xD;
&#xD;
        Exclusion Criteria:&#xD;
&#xD;
          -  Recent neoplasia (&lt; 1 year)&#xD;
&#xD;
          -  Vitamin B12 deficiency, positive serology for syphilis, thyroid function abnormalities&#xD;
             considered to be significant by the care provider.&#xD;
&#xD;
          -  Use of vitamin or mineral supplements.&#xD;
&#xD;
          -  Diagnosis of malnutrition (based on body mass index and total protein levels)&#xD;
&#xD;
          -  Metabolic syndrome or diabetes.&#xD;
&#xD;
          -  Hormonal replacement therapy.&#xD;
&#xD;
          -  Smoking&#xD;
&#xD;
          -  Chronic inflammatory disease (e.g. rheumatoid arthritis) and any other acute illness.&#xD;
      </textblock>
    </criteria>
    <gender>All</gender>
    <minimum_age>50 Years</minimum_age>
    <maximum_age>N/A</maximum_age>
    <healthy_volunteers>Accepts Healthy Volunteers</healthy_volunteers>
  </eligibility>
  <overall_official>
    <last_name>Francesco Maria Serino, M.D. PhD</last_name>
    <role>Principal Investigator</role>
    <affiliation>Doctors in Italy</affiliation>
  </overall_official>
  <overall_official>
    <last_name>Chiara Fanali, PhD</last_name>
    <role>Principal Investigator</role>
    <affiliation>University Campus Bio-Medico</affiliation>
  </overall_official>
  <overall_official>
    <last_name>Laura Dugo, PhD</last_name>
    <role>Principal Investigator</role>
    <affiliation>University Campus Bio-Medico</affiliation>
  </overall_official>
  <overall_official>
    <last_name>Simone Grasso, PhD</last_name>
    <role>Principal Investigator</role>
    <affiliation>University Campus Bio-Medico</affiliation>
  </overall_official>
  <overall_official>
    <last_name>Ettore Bergamini, M.D.</last_name>
    <role>Study Chair</role>
    <affiliation>University of Pisa</affiliation>
  </overall_official>
  <overall_official>
    <last_name>Francesca Ursini, M.D.</last_name>
    <role>Principal Investigator</role>
    <affiliation>University Campus Bio-Medico</affiliation>
  </overall_official>
  <overall_official>
    <last_name>Fabrizio Vernieri, M.D.</last_name>
    <role>Principal Investigator</role>
    <affiliation>University Campus Bio-Medico</affiliation>
  </overall_official>
  <overall_official>
    <last_name>Marina Dachà, BS.Pharm</last_name>
    <role>Study Director</role>
    <affiliation>University Campus Bio-Medico</affiliation>
  </overall_official>
  <overall_official>
    <last_name>Silvia Bernardini, M.D.</last_name>
    <role>Principal Investigator</role>
    <affiliation>University Campus Bio-Medico</affiliation>
  </overall_official>
  <overall_official>
    <last_name>Valentina Pasqualetti, PhD</last_name>
    <role>Principal Investigator</role>
    <affiliation>University Campus Bio-Medico</affiliation>
  </overall_official>
  <location>
    <facility>
      <name>Policlinico Universitario Campus Bio-Medico</name>
      <address>
        <city>Rome</city>
        <state>RM</state>
        <zip>00128</zip>
        <country>Italy</country>
      </address>
    </facility>
  </location>
  <location_countries>
    <country>Italy</country>
  </location_countries>
  <reference>
    <citation>Mangialasche F, Polidori MC, Monastero R, Ercolani S, Camarda C, Cecchetti R, Mecocci P. Biomarkers of oxidative and nitrosative damage in Alzheimer's disease and mild cognitive impairment. Ageing Res Rev. 2009 Oct;8(4):285-305. doi: 10.1016/j.arr.2009.04.002. Epub 2009 Apr 17.</citation>
    <PMID>19376275</PMID>
  </reference>
  <reference>
    <citation>Markesbery WR. Oxidative stress hypothesis in Alzheimer's disease. Free Radic Biol Med. 1997;23(1):134-47. doi: 10.1016/s0891-5849(96)00629-6.</citation>
    <PMID>9165306</PMID>
  </reference>
  <reference>
    <citation>Perry G, Nunomura A, Hirai K, Zhu X, Perez M, Avila J, Castellani RJ, Atwood CS, Aliev G, Sayre LM, Takeda A, Smith MA. Is oxidative damage the fundamental pathogenic mechanism of Alzheimer's and other neurodegenerative diseases? Free Radic Biol Med. 2002 Dec 1;33(11):1475-9. doi: 10.1016/s0891-5849(02)01113-9.</citation>
    <PMID>12446204</PMID>
  </reference>
  <reference>
    <citation>Mecocci P. Oxidative stress in mild cognitive impairment and Alzheimer disease: a continuum. J Alzheimers Dis. 2004 Apr;6(2):159-63. doi: 10.3233/jad-2004-6207.</citation>
    <PMID>15096699</PMID>
  </reference>
  <reference>
    <citation>Polidori MC, Mecocci P. Plasma susceptibility to free radical-induced antioxidant consumption and lipid peroxidation is increased in very old subjects with Alzheimer disease. J Alzheimers Dis. 2002 Dec;4(6):517-22. doi: 10.3233/jad-2002-4608.</citation>
    <PMID>12629261</PMID>
  </reference>
  <reference>
    <citation>Galbusera C, Facheris M, Magni F, Galimberti G, Sala G, Tremolada L, Isella V, Guerini FR, Appollonio I, Galli-Kienle M, Ferrarese C. Increased susceptibility to plasma lipid peroxidation in Alzheimer disease patients. Curr Alzheimer Res. 2004 May;1(2):103-9. doi: 10.2174/1567205043332171.</citation>
    <PMID>15975074</PMID>
  </reference>
  <reference>
    <citation>Casado A, Encarnacion Lopez-Fernandez M, Concepcion Casado M, de La Torre R. Lipid peroxidation and antioxidant enzyme activities in vascular and Alzheimer dementias. Neurochem Res. 2008 Mar;33(3):450-8. doi: 10.1007/s11064-007-9453-3. Epub 2007 Aug 25.</citation>
    <PMID>17721818</PMID>
  </reference>
  <reference>
    <citation>Serra JA, Dominguez RO, de Lustig ES, Guareschi EM, Famulari AL, Bartolome EL, Marschoff ER. Parkinson's disease is associated with oxidative stress: comparison of peripheral antioxidant profiles in living Parkinson's, Alzheimer's and vascular dementia patients. J Neural Transm (Vienna). 2001;108(10):1135-48. doi: 10.1007/s007020170003.</citation>
    <PMID>11725816</PMID>
  </reference>
  <reference>
    <citation>Kawamoto EM, Munhoz CD, Glezer I, Bahia VS, Caramelli P, Nitrini R, Gorjao R, Curi R, Scavone C, Marcourakis T. Oxidative state in platelets and erythrocytes in aging and Alzheimer's disease. Neurobiol Aging. 2005 Jun;26(6):857-64. doi: 10.1016/j.neurobiolaging.2004.08.011.</citation>
    <PMID>15718044</PMID>
  </reference>
  <reference>
    <citation>Bermejo P, Gomez-Serranillos P, Santos J, Pastor E, Gil P, Martin-Aragon S. Determination of malonaldehyde in Alzheimer's disease: a comparative study of high-performance liquid chromatography and thiobarbituric acid test. Gerontology. 1997;43(4):218-22. doi: 10.1159/000213853.</citation>
    <PMID>9222750</PMID>
  </reference>
  <reference>
    <citation>Baldeiras I, Santana I, Proenca MT, Garrucho MH, Pascoal R, Rodrigues A, Duro D, Oliveira CR. Peripheral oxidative damage in mild cognitive impairment and mild Alzheimer's disease. J Alzheimers Dis. 2008 Sep;15(1):117-28. doi: 10.3233/jad-2008-15110.</citation>
    <PMID>18780972</PMID>
  </reference>
  <reference>
    <citation>Torres LL, Quaglio NB, de Souza GT, Garcia RT, Dati LM, Moreira WL, Loureiro AP, de Souza-Talarico JN, Smid J, Porto CS, Bottino CM, Nitrini R, Barros SB, Camarini R, Marcourakis T. Peripheral oxidative stress biomarkers in mild cognitive impairment and Alzheimer's disease. J Alzheimers Dis. 2011;26(1):59-68. doi: 10.3233/JAD-2011-110284.</citation>
    <PMID>21593563</PMID>
  </reference>
  <reference>
    <citation>Onaran I, Yalcin AS, Sultuybek G. Effect of donor age on the susceptibility of erythrocytes and erythrocyte membranes to cumene hydroperoxide-induced oxidative stress. Mech Ageing Dev. 1997 Nov;98(2):127-38. doi: 10.1016/s0047-6374(97)00078-x.</citation>
    <PMID>9379709</PMID>
  </reference>
  <reference>
    <citation>Garcia-Arumi E, Andreu AL, Lopez-Hellin J, Schwartz S. Effect of oxidative stress on lymphocytes from elderly subjects. Clin Sci (Lond). 1998 Apr;94(4):447-52. doi: 10.1042/cs0940447.</citation>
    <PMID>9640351</PMID>
  </reference>
  <reference>
    <citation>Davis KL, Davis BM, Greenwald BS, Mohs RC, Mathe AA, Johns CA, Horvath TB. Cortisol and Alzheimer's disease, I: Basal studies. Am J Psychiatry. 1986 Mar;143(3):300-5. doi: 10.1176/ajp.143.3.300.</citation>
    <PMID>3953862</PMID>
  </reference>
  <reference>
    <citation>Costantini D, Marasco V, Moller AP. A meta-analysis of glucocorticoids as modulators of oxidative stress in vertebrates. J Comp Physiol B. 2011 May;181(4):447-56. doi: 10.1007/s00360-011-0566-2. Epub 2011 Mar 18.</citation>
    <PMID>21416253</PMID>
  </reference>
  <reference>
    <citation>Joergensen A, Broedbaek K, Weimann A, Semba RD, Ferrucci L, Joergensen MB, Poulsen HE. Association between urinary excretion of cortisol and markers of oxidatively damaged DNA and RNA in humans. PLoS One. 2011;6(6):e20795. doi: 10.1371/journal.pone.0020795. Epub 2011 Jun 7.</citation>
    <PMID>21687734</PMID>
  </reference>
  <verification_date>March 2018</verification_date>
  <study_first_submitted>October 1, 2012</study_first_submitted>
  <study_first_submitted_qc>October 15, 2012</study_first_submitted_qc>
  <study_first_posted type="Estimate">October 16, 2012</study_first_posted>
  <last_update_submitted>January 22, 2020</last_update_submitted>
  <last_update_submitted_qc>January 22, 2020</last_update_submitted_qc>
  <last_update_posted type="Actual">January 23, 2020</last_update_posted>
  <responsible_party>
    <responsible_party_type>Sponsor-Investigator</responsible_party_type>
    <investigator_affiliation>Campus Bio-Medico University</investigator_affiliation>
    <investigator_full_name>Raffaele Antonelli Incalzi</investigator_full_name>
    <investigator_title>Professor</investigator_title>
  </responsible_party>
  <keyword>Alzheimer's disease</keyword>
  <keyword>Oxidative stress</keyword>
  <keyword>HPA axis</keyword>
  <condition_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Alzheimer Disease</mesh_term>
    <mesh_term>Adrenocortical Hyperfunction</mesh_term>
  </condition_browse>
  <patient_data>
    <sharing_ipd>No</sharing_ipd>
  </patient_data>
  <!-- Results have not yet been posted for this study                                          -->
</clinical_study>


download date: ClinicalTrials.gov processed this data on September 20, 2023
link text: Link to the current ClinicalTrials.gov record.
url: https://clinicaltrials.gov/ct2/show/NCT01707719
org study id: ERASE
nct id: NCT01707719
lead sponsor: 
has dmc: Yes
High lipid peroxidation and altered antioxidant defenses have been frequently reported in
      Alzheimer's disease patients.

      The purpose of this study is to investigate susceptibility to photo-oxidation of isolated
      erythrocyte membranes, in patients affected by Alzheimer's disease and age- and sex-matched,
      non demented subjects.
The study hypothesis is that high lipid peroxidation and decreased antioxidant defenses
      characterize the natural history of Alzheimer's disease.

      It will be evaluated the release of malondialdehyde (MDA) from ex-vivo photo-oxidized
      erythrocyte ghosts, through a very easy and convenient lab procedure for the preparation of
      erythrocyte membrane samples.

      Isolated and purified red blood cell membranes will be in vitro exposed to oxidative stress
      by UV-B radiation. The extent of cell membrane damage will be quantified by the fluorometric
      determination of MDA.

      Induction of oxidative stress through ultraviolet rays, unlike that obtained by chemical
      oxidizing agents, is fully controllable, since it produces effects only during irradiation.
      Moreover, using isolated erythrocyte membranes allows for a greater specificity in the
      evaluation of MDA produced, and reduces the amount of blood required for the assay.

      A portion of the blood sample (500 µL) will be sent to the laboratory of Lipinutragen
      (spin-off of CNR- National Research Center Bologna, Italy) where an erythrocyte membrane
      lipidomic analysis will be performed for the characterization of membrane phospholipids, in
      order to determinate the different lipid components (saturated fatty acids, monounsaturated
      and polyunsaturated, trans fatty acids), each one characterized by a different oxidative
      reactivity.

      Recently published papers showed a striking association between urinary excretion of cortisol
      and the increase of some markers of oxidative damage of DNA and RNA (in humans). This finding
      provides further support to the idea that chronic psychological stress, who is associated to
      hypercortisolemia, can lead to an acceleration of the aging process.

      The brain is a major target of the effects of glucocorticoids (CCS). The harmful consequences
      of cortisol on the hippocampus (one of the first brain areas affected by Alzheimer's disease)
      are well known. Some studies showed inverse correlations between cortisol levels and
      neuropsychological performance in patients with depression, dementia as well as in people
      treated chronically with CCS.

      Alzheimer's disease is associated with states of hypercortisolism. Nonetheless, so far, its
      correlation with the level of oxidative stress has not been studied. We will investigate the
      relationship between 24h excretion of urinary cortisol and the level of malondialdehyde,
      produced by isolated and purified red blood cell membranes, in vitro exposed to oxidative
      stress by UV-B radiation.
observational model: Case-Control
time perspective: Cross-Sectional
measure: Malondialdehyde assay
time frame: At the time of recruitment
description: Isolated and purified red blood cell membranes will be in vitro exposed to oxidative stress by UV-B radiation. The extent of cell membrane damage will be quantified by the fluorometric determination of malondialdehyde.
measure: Relationship between urinary excretion of cortisol and levels of malondialdehyde
time frame: At the time of recruitment
description: Hyperactivity of the hypothalamic pituitary adrenal axis has been frequently described in Alzheimer's disease. Recently published work reported an association between high secretion of cortisol and oxidative stress. We will investigate the relationship between 24 h excretion of urinary cortisol and the level of malondialdehyde, produced by isolated and purified red blood cell membranes, in vitro exposed to oxidative stress by UV-B radiation.
arm group label: Alzheimer's disease
arm group label: Non demented subjects
Whole blood
study pop: 
sampling method: Probability Sample
criteria: 
gender: All
minimum age: 50 Years
maximum age: N/A
healthy volunteers: Accepts Healthy Volunteers
last name: Francesco Maria Serino, M.D. PhD
role: Principal Investigator
affiliation: Doctors in Italy
last name: Chiara Fanali, PhD
role: Principal Investigator
affiliation: University Campus Bio-Medico
last name: Laura Dugo, PhD
role: Principal Investigator
affiliation: University Campus Bio-Medico
last name: Simone Grasso, PhD
role: Principal Investigator
affiliation: University Campus Bio-Medico
last name: Ettore Bergamini, M.D.
role: Study Chair
affiliation: University of Pisa
last name: Francesca Ursini, M.D.
role: Principal Investigator
affiliation: University Campus Bio-Medico
last name: Fabrizio Vernieri, M.D.
role: Principal Investigator
affiliation: University Campus Bio-Medico
last name: Marina Dachà, BS.Pharm
role: Study Director
affiliation: University Campus Bio-Medico
last name: Silvia Bernardini, M.D.
role: Principal Investigator
affiliation: University Campus Bio-Medico
last name: Valentina Pasqualetti, PhD
role: Principal Investigator
affiliation: University Campus Bio-Medico
facility: 
country: Italy
citation: Mangialasche F, Polidori MC, Monastero R, Ercolani S, Camarda C, Cecchetti R, Mecocci P. Biomarkers of oxidative and nitrosative damage in Alzheimer's disease and mild cognitive impairment. Ageing Res Rev. 2009 Oct;8(4):285-305. doi: 10.1016/j.arr.2009.04.002. Epub 2009 Apr 17.
PMID: 19376275
citation: Markesbery WR. Oxidative stress hypothesis in Alzheimer's disease. Free Radic Biol Med. 1997;23(1):134-47. doi: 10.1016/s0891-5849(96)00629-6.
PMID: 9165306
citation: Perry G, Nunomura A, Hirai K, Zhu X, Perez M, Avila J, Castellani RJ, Atwood CS, Aliev G, Sayre LM, Takeda A, Smith MA. Is oxidative damage the fundamental pathogenic mechanism of Alzheimer's and other neurodegenerative diseases? Free Radic Biol Med. 2002 Dec 1;33(11):1475-9. doi: 10.1016/s0891-5849(02)01113-9.
PMID: 12446204
citation: Mecocci P. Oxidative stress in mild cognitive impairment and Alzheimer disease: a continuum. J Alzheimers Dis. 2004 Apr;6(2):159-63. doi: 10.3233/jad-2004-6207.
PMID: 15096699
citation: Polidori MC, Mecocci P. Plasma susceptibility to free radical-induced antioxidant consumption and lipid peroxidation is increased in very old subjects with Alzheimer disease. J Alzheimers Dis. 2002 Dec;4(6):517-22. doi: 10.3233/jad-2002-4608.
PMID: 12629261
citation: Galbusera C, Facheris M, Magni F, Galimberti G, Sala G, Tremolada L, Isella V, Guerini FR, Appollonio I, Galli-Kienle M, Ferrarese C. Increased susceptibility to plasma lipid peroxidation in Alzheimer disease patients. Curr Alzheimer Res. 2004 May;1(2):103-9. doi: 10.2174/1567205043332171.
PMID: 15975074
citation: Casado A, Encarnacion Lopez-Fernandez M, Concepcion Casado M, de La Torre R. Lipid peroxidation and antioxidant enzyme activities in vascular and Alzheimer dementias. Neurochem Res. 2008 Mar;33(3):450-8. doi: 10.1007/s11064-007-9453-3. Epub 2007 Aug 25.
PMID: 17721818
citation: Serra JA, Dominguez RO, de Lustig ES, Guareschi EM, Famulari AL, Bartolome EL, Marschoff ER. Parkinson's disease is associated with oxidative stress: comparison of peripheral antioxidant profiles in living Parkinson's, Alzheimer's and vascular dementia patients. J Neural Transm (Vienna). 2001;108(10):1135-48. doi: 10.1007/s007020170003.
PMID: 11725816
citation: Kawamoto EM, Munhoz CD, Glezer I, Bahia VS, Caramelli P, Nitrini R, Gorjao R, Curi R, Scavone C, Marcourakis T. Oxidative state in platelets and erythrocytes in aging and Alzheimer's disease. Neurobiol Aging. 2005 Jun;26(6):857-64. doi: 10.1016/j.neurobiolaging.2004.08.011.
PMID: 15718044
citation: Bermejo P, Gomez-Serranillos P, Santos J, Pastor E, Gil P, Martin-Aragon S. Determination of malonaldehyde in Alzheimer's disease: a comparative study of high-performance liquid chromatography and thiobarbituric acid test. Gerontology. 1997;43(4):218-22. doi: 10.1159/000213853.
PMID: 9222750
citation: Baldeiras I, Santana I, Proenca MT, Garrucho MH, Pascoal R, Rodrigues A, Duro D, Oliveira CR. Peripheral oxidative damage in mild cognitive impairment and mild Alzheimer's disease. J Alzheimers Dis. 2008 Sep;15(1):117-28. doi: 10.3233/jad-2008-15110.
PMID: 18780972
citation: Torres LL, Quaglio NB, de Souza GT, Garcia RT, Dati LM, Moreira WL, Loureiro AP, de Souza-Talarico JN, Smid J, Porto CS, Bottino CM, Nitrini R, Barros SB, Camarini R, Marcourakis T. Peripheral oxidative stress biomarkers in mild cognitive impairment and Alzheimer's disease. J Alzheimers Dis. 2011;26(1):59-68. doi: 10.3233/JAD-2011-110284.
PMID: 21593563
citation: Onaran I, Yalcin AS, Sultuybek G. Effect of donor age on the susceptibility of erythrocytes and erythrocyte membranes to cumene hydroperoxide-induced oxidative stress. Mech Ageing Dev. 1997 Nov;98(2):127-38. doi: 10.1016/s0047-6374(97)00078-x.
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responsible party type: Sponsor-Investigator
investigator affiliation: Campus Bio-Medico University
investigator full name: Raffaele Antonelli Incalzi
investigator title: Professor
mesh term: Alzheimer Disease
mesh term: Adrenocortical Hyperfunction
sharing ipd: No