دورية أكاديمية

Decreased levels of BDNF protein in Alzheimer temporal cortex are independent of BDNF polymorphisms.

التفاصيل البيبلوغرافية
العنوان: Decreased levels of BDNF protein in Alzheimer temporal cortex are independent of BDNF polymorphisms.
المؤلفون: Lee J; Harvard Medical School, Massachusetts General Hospital, 114 16th Street, Charlestown, MA 02129, USA., Fukumoto H, Orne J, Klucken J, Raju S, Vanderburg CR, Irizarry MC, Hyman BT, Ingelsson M
المصدر: Experimental neurology [Exp Neurol] 2005 Jul; Vol. 194 (1), pp. 91-6.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
اللغة: English
بيانات الدورية: Publisher: Academic Press Country of Publication: United States NLM ID: 0370712 Publication Model: Print Cited Medium: Print ISSN: 0014-4886 (Print) Linking ISSN: 00144886 NLM ISO Abbreviation: Exp Neurol Subsets: MEDLINE
أسماء مطبوعة: Publication: Orlando Fl : Academic Press
Original Publication: New York.
مواضيع طبية MeSH: Alzheimer Disease/*genetics , Alzheimer Disease/*metabolism , Brain-Derived Neurotrophic Factor/*genetics , Brain-Derived Neurotrophic Factor/*metabolism , Polymorphism, Genetic/*genetics , Temporal Lobe/*metabolism, Aged ; Alzheimer Disease/pathology ; Apolipoprotein E4 ; Apolipoproteins E/genetics ; Biomarkers/metabolism ; Cerebellum/metabolism ; Cohort Studies ; DNA Mutational Analysis ; Down-Regulation/physiology ; Female ; Gene Frequency ; Genetic Predisposition to Disease/genetics ; Genetic Testing ; Genotype ; Hippocampus/metabolism ; Hippocampus/pathology ; Humans ; Male ; Neurons/metabolism ; Neurons/pathology ; Plaque, Amyloid/genetics ; Plaque, Amyloid/metabolism ; Plaque, Amyloid/pathology ; Synaptophysin/metabolism ; Temporal Lobe/pathology
مستخلص: Levels of brain-derived neurotrophic factor (BDNF) are reduced in specific brain regions in Alzheimer's disease (AD) and BDNF gene polymorphisms have been suggested to influence AD risk, hippocampal function, and memory. We investigated whether the polymorphisms at the BDNF 196 and 270 loci were associated with AD in a clinical and neuropathological cohort of 116 AD cases and 77 control subjects. To determine how BDNF protein levels relate to BDNF polymorphisms and AD pathology, we also measured BDNF in temporal association cortex, frontal association cortex, and cerebellum in 57 of the AD and 21 control cases. BDNF protein levels in temporal neocortex of the AD brains were reduced by 33% compared to control brains, whereas levels were unchanged in frontal and cerebellar cortex. The BDNF genotypes were not significantly associated with a diagnosis of AD, although the BDNF 270 C allele was slightly overrepresented among carriers of the APOEepsilon4 allele. Moreover, BDNF protein levels did not differ between the various BDNF genotypes and alleles. Neuropathologically, the loss of BDNF in AD showed a weak correlation with accumulation of neuritic amyloid plaques and loss of the neuronal/synaptic marker synaptophysin. The results suggest that the investigated BDNF polymorphisms are neither robust genetic risk factors nor determinants of BDNF protein levels in AD.
معلومات مُعتمدة: AG 05134 United States AG NIA NIH HHS
المشرفين على المادة: 0 (Apolipoprotein E4)
0 (Apolipoproteins E)
0 (Biomarkers)
0 (Brain-Derived Neurotrophic Factor)
0 (Synaptophysin)
تواريخ الأحداث: Date Created: 20050519 Date Completed: 20050715 Latest Revision: 20151119
رمز التحديث: 20231215
DOI: 10.1016/j.expneurol.2005.01.026
PMID: 15899246
قاعدة البيانات: MEDLINE
الوصف
تدمد:0014-4886
DOI:10.1016/j.expneurol.2005.01.026