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      Call for Papers: Sex and Gender in Neurodegenerative Diseases

      Submit here before September 30, 2024

      About Neurodegenerative Diseases: 3.0 Impact Factor I 4.3 CiteScore I 0.695 Scimago Journal & Country Rank (SJR)

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      Brain-Derived Neurotrophic Factor Serum Levels and Hippocampal Volume in Mild Cognitive Impairment and Dementia due to Alzheimer Disease

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          Abstract

          Background/Aims: Hippocampal atrophy is a recognized biomarker of Alzheimer disease (AD) pathology. Serum brain-derived neurotrophic factor (BDNF) reduction has been associated with neurodegeneration. We aimed to evaluate BDNF serum levels and hippocampal volume in clinical AD (dementia and mild cognitive impairment [MCI]). Methods: Participants were 10 patients with MCI and 13 with dementia due to AD as well as 10 healthy controls. BDNF serum levels were determined by ELISA and volumetric measures with NeuroQuant®. Results: MCI and dementia patients presented lower BDNF serum levels than healthy participants; dementia patients presented a smaller hippocampal volume than MCI patients and healthy participants. Discussion: The findings support that the decrease in BDNF might start before the establishment of neuronal injury expressed by the hippocampal reduction.

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          Neuroprotective effects of brain-derived neurotrophic factor in rodent and primate models of Alzheimer's disease.

          Alan Nagahara, David Merrill, Giovanni Coppola … (2009)
          Profound neuronal dysfunction in the entorhinal cortex contributes to early loss of short-term memory in Alzheimer's disease. Here we show broad neuroprotective effects of entorhinal brain-derived neurotrophic factor (BDNF) administration in several animal models of Alzheimer's disease, with extension of therapeutic benefits into the degenerating hippocampus. In amyloid-transgenic mice, BDNF gene delivery, when administered after disease onset, reverses synapse loss, partially normalizes aberrant gene expression, improves cell signaling and restores learning and memory. These outcomes occur independently of effects on amyloid plaque load. In aged rats, BDNF infusion reverses cognitive decline, improves age-related perturbations in gene expression and restores cell signaling. In adult rats and primates, BDNF prevents lesion-induced death of entorhinal cortical neurons. In aged primates, BDNF reverses neuronal atrophy and ameliorates age-related cognitive impairment. Collectively, these findings indicate that BDNF exerts substantial protective effects on crucial neuronal circuitry involved in Alzheimer's disease, acting through amyloid-independent mechanisms. BDNF therapeutic delivery merits exploration as a potential therapy for Alzheimer's disease.
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            Trajectories of brain aging in middle-aged and older adults: regional and individual differences.

            Ulman Lindenberger, Naftali Raz, Julie K. Kennedy … (2010)
            The human brain changes with age. However, the rate and the trajectories of change vary among the brain regions and among individuals, and the reasons for these differences are unclear. In a sample of healthy middle-aged and older adults, we examined mean volume change and individual differences in the rate of change in 12 regional brain volumes over approximately 30 months. In addition to the baseline assessment, there were two follow-ups, 15 months apart. We observed significant average shrinkage of the hippocampus, entorhinal cortex, orbital-frontal cortex, and cerebellum in each of the intervals. Shrinkage of the hippocampus accelerated with time, whereas shrinkage of the caudate nucleus, prefrontal subcortical white matter, and corpus callosum emerged only at the second follow-up. Throughout both assessment intervals, the mean volumes of the lateral prefrontal and primary visual cortices, putamen, and pons did not change. Significant individual differences in shrinkage rates were observed in the lateral prefrontal cortex, the cerebellum, and all the white matter regions throughout the study, whereas additional regions (medial-temporal structures, the insula, and the basal ganglia) showed significant individual variation in change during the second follow-up. No individual variability was noted in the change of orbital frontal and visual cortices. In two white matter regions, we were able to identify factors associated with individual differences in brain shrinkage. In corpus callosum, shrinkage rate was greater in persons with hypertension, and in the pons, women and carriers of the ApoEepsilon4 allele exhibited declines not noted in the whole sample. Copyright 2010 Elsevier Inc. All rights reserved.
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              [Suggestions for utilization of the mini-mental state examination in Brazil].

              Sonia M D Brucki, Ricardo Nitrini, Paulo Caramelli … (2003)
              Mini-metal state examination (MMSE) is a screening test to detect cognitive impairment. The objectives of the present study are to describe some adaptations for use of MMSE in Brazil and to propose rules for its uniform application. We evaluated 433 healthy subjects using the MMSE and verified the possible influence of demographic variables on total scores. Educational level was the main factor that influenced performance, demonstrated by ANOVA: F(4,425) = 100.45, p<0.0001. The median values for educational groups were: 20 for illiterates; 25 for 1 to 4 yrs; 26.5 for 5 to 8 yrs; 28 for 9 to 11 yrs and 29 for higher levels. The MMSE is an excellent screening instrument and definitive rules are necessary for comparison purposes.
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                Author and article information

                Journal
                Journal ID (publisher-id): DEE
                Journal ID (pmc): DEE
                Journal ID (doi): 10.1159/issn.1664-5464
                Title: Dementia and Geriatric Cognitive Disorders Extra
                Publisher: S. Karger AG
                ISSN (Electronic): 1664-5464
                Publication date Subscription-year: 2016
                Publication date Collection: September – December 2016
                Publication date (Electronic): 09 December 2016
                Volume: 6
                Issue: 3
                Pages: 559-567
                Affiliations
                aDementia Clinic, Neurology Service, bBipolar Disorder Program, Laboratory of Molecular Psychiatry, and cRadiology Service, Hospital de Clínicas de Porto Alegre (HCPA), dPostgraduate Program in Medical Sciences, School of Medicine, and eInternal Medicine Department, School of Medicine, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, Brazil
                Author notes
                *Márcia L.F. Chaves, Rua Ramiro Barcelos, 2350, sala 2040, Porto Alegre, RS 90035-091 (Brazil), E-Mail mchaves@hcpa.edu.br
                Article
                Publisher ID: 450601 Pmcid ID: PMC5216193 Other ID: Dement Geriatr Cogn Disord Extra 2016;6:559-567
                DOI: 10.1159/000450601
                PMC ID: PMC5216193
                PubMed ID: 28101102
                SO-VID: e541dc01-a61e-4135-aefe-94a9a169413a
                Copyright © © 2016 The Author(s) Published by S. Karger AG, Basel
                License:

                This article is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND). Usage and distribution for commercial purposes as well as any distribution of modified material requires written permission. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Page count
                Tables: 2, References: 50, Pages: 9
                Categories
                Subject: Original Research Article

                ScienceOpen disciplines: Geriatric medicine,Neurology,Cardiovascular Medicine,Neurosciences,Clinical Psychology & Psychiatry,Public health
                Keywords: Alzheimer disease,Blood biomarker,Mild cognitive impairment,Brain atrophy,Hippocampus
                Data availability:
                ScienceOpen disciplines: Geriatric medicine, Neurology, Cardiovascular Medicine, Neurosciences, Clinical Psychology & Psychiatry, Public health
                Keywords: Alzheimer disease, Blood biomarker, Mild cognitive impairment, Brain atrophy, Hippocampus

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