Marked disparity between age‐related changes in dopamine and other presynaptic dopaminergic markers in human striatum
Because age‐related changes in brain dopaminergic innervation are assumed to influence human disorders involving dopamine (DA), we measured the levels of several presynpatic DAergic markers [DA, homovanillic acid, tyrosine hydroxylase (TH), aromatic l‐amino acid decarboxylase (AADC), vesicular monoa...
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| Published in | Journal of neurochemistry Vol. 87; no. 3; pp. 574 - 585 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford, UK
Blackwell Science Ltd
01.11.2003
Blackwell |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0022-3042 1471-4159 |
| DOI | 10.1046/j.1471-4159.2003.02017.x |
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| Abstract | Because age‐related changes in brain dopaminergic innervation are assumed to influence human disorders involving dopamine (DA), we measured the levels of several presynpatic DAergic markers [DA, homovanillic acid, tyrosine hydroxylase (TH), aromatic l‐amino acid decarboxylase (AADC), vesicular monoamine transporter 2 (VMAT2), and dopamine transporter (DAT)] in post‐mortem human striatum (caudate and putamen) from 56 neurologically normal subjects aged 1 day to 103 years. Striatal DA levels exhibited pronounced (2‐ to 3‐fold) post‐natal increases through adolescence and then decreases during aging. Similarly, TH and AADC increased almost 100% during the first 2 post‐natal years; however, the levels of TH and, to a lesser extent, AADC then declined to adult levels by approximately 30 years of age. Although VMAT2 and DAT levels closely paralleled those of TH, resulting in relatively constant TH to transporter ratios during development and aging, a modest but significant decline (13%) in DAT levels was observed in only caudate during aging. This biphasic post‐natal pattern of the presynaptic markers suggests that striatal DAergic innervation/neuropil appears to continue to develop well past birth but appears to become overelaborated and undergo regressive remodeling during adolescence. However, during adulthood, a striking discrepancy was observed between the loss of DA and the relative preservation of proteins involved in its biosynthesis and compartmentation. This suggests that declines in DA‐related function during adulthood and senescence may be explained by losses in DA per se as opposed to DAergic neuropil. |
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| AbstractList | Because age‐related changes in brain dopaminergic innervation are assumed to influence human disorders involving dopamine (DA), we measured the levels of several presynpatic DAergic markers [DA, homovanillic acid, tyrosine hydroxylase (TH), aromatic l‐amino acid decarboxylase (AADC), vesicular monoamine transporter 2 (VMAT2), and dopamine transporter (DAT)] in post‐mortem human striatum (caudate and putamen) from 56 neurologically normal subjects aged 1 day to 103 years. Striatal DA levels exhibited pronounced (2‐ to 3‐fold) post‐natal increases through adolescence and then decreases during aging. Similarly, TH and AADC increased almost 100% during the first 2 post‐natal years; however, the levels of TH and, to a lesser extent, AADC then declined to adult levels by approximately 30 years of age. Although VMAT2 and DAT levels closely paralleled those of TH, resulting in relatively constant TH to transporter ratios during development and aging, a modest but significant decline (13%) in DAT levels was observed in only caudate during aging. This biphasic post‐natal pattern of the presynaptic markers suggests that striatal DAergic innervation/neuropil appears to continue to develop well past birth but appears to become overelaborated and undergo regressive remodeling during adolescence. However, during adulthood, a striking discrepancy was observed between the loss of DA and the relative preservation of proteins involved in its biosynthesis and compartmentation. This suggests that declines in DA‐related function during adulthood and senescence may be explained by losses in DA per se as opposed to DAergic neuropil. Because age‐related changes in brain dopaminergic innervation are assumed to influence human disorders involving dopamine (DA), we measured the levels of several presynpatic DAergic markers [DA, homovanillic acid, tyrosine hydroxylase (TH), aromatic l ‐amino acid decarboxylase (AADC), vesicular monoamine transporter 2 (VMAT2), and dopamine transporter (DAT)] in post‐mortem human striatum (caudate and putamen) from 56 neurologically normal subjects aged 1 day to 103 years. Striatal DA levels exhibited pronounced (2‐ to 3‐fold) post‐natal increases through adolescence and then decreases during aging. Similarly, TH and AADC increased almost 100% during the first 2 post‐natal years; however, the levels of TH and, to a lesser extent, AADC then declined to adult levels by approximately 30 years of age. Although VMAT2 and DAT levels closely paralleled those of TH, resulting in relatively constant TH to transporter ratios during development and aging, a modest but significant decline (13%) in DAT levels was observed in only caudate during aging. This biphasic post‐natal pattern of the presynaptic markers suggests that striatal DAergic innervation/neuropil appears to continue to develop well past birth but appears to become overelaborated and undergo regressive remodeling during adolescence. However, during adulthood, a striking discrepancy was observed between the loss of DA and the relative preservation of proteins involved in its biosynthesis and compartmentation. This suggests that declines in DA‐related function during adulthood and senescence may be explained by losses in DA per se as opposed to DAergic neuropil. Because age-related changes in brain dopaminergic innervation are assumed to influence human disorders involving dopamine (DA), we measured the levels of several presynpatic DAergic markers [DA, homovanillic acid, tyrosine hydroxylase (TH), aromatic L-amino acid decarboxylase (AADC), vesicular monoamine transporter 2 (VMAT2), and dopamine transporter (DAT)] in post-mortem human striatum (caudate and putamen) from 56 neurologically normal subjects aged 1 day to 103 years. Striatal DA levels exhibited pronounced (2- to 3-fold) post-natal increases through adolescence and then decreases during aging. Similarly, TH and AADC increased almost 100% during the first 2 post-natal years; however, the levels of TH and, to a lesser extent, AADC then declined to adult levels by approximately 30 years of age. Although VMAT2 and DAT levels closely paralleled those of TH, resulting in relatively constant TH to transporter ratios during development and aging, a modest but significant decline (13%) in DAT levels was observed in only caudate during aging. This biphasic post-natal pattern of the presynaptic markers suggests that striatal DAergic innervation/neuropil appears to continue to develop well past birth but appears to become overelaborated and undergo regressive remodeling during adolescence. However, during adulthood, a striking discrepancy was observed between the loss of DA and the relative preservation of proteins involved in its biosynthesis and compartmentation. This suggests that declines in DA-related function during adulthood and senescence may be explained by losses in DA per se as opposed to DAergic neuropil.Because age-related changes in brain dopaminergic innervation are assumed to influence human disorders involving dopamine (DA), we measured the levels of several presynpatic DAergic markers [DA, homovanillic acid, tyrosine hydroxylase (TH), aromatic L-amino acid decarboxylase (AADC), vesicular monoamine transporter 2 (VMAT2), and dopamine transporter (DAT)] in post-mortem human striatum (caudate and putamen) from 56 neurologically normal subjects aged 1 day to 103 years. Striatal DA levels exhibited pronounced (2- to 3-fold) post-natal increases through adolescence and then decreases during aging. Similarly, TH and AADC increased almost 100% during the first 2 post-natal years; however, the levels of TH and, to a lesser extent, AADC then declined to adult levels by approximately 30 years of age. Although VMAT2 and DAT levels closely paralleled those of TH, resulting in relatively constant TH to transporter ratios during development and aging, a modest but significant decline (13%) in DAT levels was observed in only caudate during aging. This biphasic post-natal pattern of the presynaptic markers suggests that striatal DAergic innervation/neuropil appears to continue to develop well past birth but appears to become overelaborated and undergo regressive remodeling during adolescence. However, during adulthood, a striking discrepancy was observed between the loss of DA and the relative preservation of proteins involved in its biosynthesis and compartmentation. This suggests that declines in DA-related function during adulthood and senescence may be explained by losses in DA per se as opposed to DAergic neuropil. Because age-related changes in brain dopaminergic innervation are assumed to influence human disorders involving dopamine (DA), we measured the levels of several presynpatic DAergic markers [DA, homovanillic acid, tyrosine hydroxylase (TH), aromatic L-amino acid decarboxylase (AADC), vesicular monoamine transporter 2 (VMAT2), and dopamine transporter (DAT)] in post-mortem human striatum (caudate and putamen) from 56 neurologically normal subjects aged 1 day to 103 years. Striatal DA levels exhibited pronounced (2- to 3-fold) post-natal increases through adolescence and then decreases during aging. Similarly, TH and AADC increased almost 100% during the first 2 post-natal years; however, the levels of TH and, to a lesser extent, AADC then declined to adult levels by approximately 30 years of age. Although VMAT2 and DAT levels closely paralleled those of TH, resulting in relatively constant TH to transporter ratios during development and aging, a modest but significant decline (13%) in DAT levels was observed in only caudate during aging. This biphasic postnatal pattern of the presynaptic markers suggests that striatal DAergic innervation/neuropil appears to continue to develop well past birth but appears to become overelaborated and undergo regressive remodeling during adolescence. However, during adulthood, a striking discrepancy was observed between the loss of DA and the relative preservation of proteins involved in its biosynthesis and compartmentation. This suggests that declines in DA-related function during adulthood and senescence may be explained by losses in DA per se as opposed to DAergic neuropil. |
| Author | Haycock, John W. Becker, Laurence Hornykiewicz, Oleh Ang, Lee Kish, Stephen J. Furukawa, Yoshiaki |
| Author_xml | – sequence: 1 givenname: John W. surname: Haycock fullname: Haycock, John W. – sequence: 2 givenname: Laurence surname: Becker fullname: Becker, Laurence – sequence: 3 givenname: Lee surname: Ang fullname: Ang, Lee – sequence: 4 givenname: Yoshiaki surname: Furukawa fullname: Furukawa, Yoshiaki – sequence: 5 givenname: Oleh surname: Hornykiewicz fullname: Hornykiewicz, Oleh – sequence: 6 givenname: Stephen J. surname: Kish fullname: Kish, Stephen J. |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15231357$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/14535941$$D View this record in MEDLINE/PubMed |
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| Keywords | Senescence blot immunolabeling Central nervous system Lyases Biosynthesis Tyrosine 3-monooxygenase Encephalon Carboxy-lyases Development Age Vesicular monoamine transporter aromatic L-amino acid decarboxylase Human Dopamine vesicular monoamine transporter 2 Enzyme Postmortem Basal ganglion Corpus striatum Catecholamine Putamen tyrosine hydroxylase Carbon-carbon lyases dopamine transporter Neurotransmitter Aromatic-L-amino-acid decarboxylase Dopaminergic neuron Oxidoreductases Presynaptic nerve ending |
| Language | English |
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| PublicationDate | November 2003 |
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| References | 1991; 114 1989; 86 1974; 97 1991; 12 1991; 56 2000; 47 1995; 38 1993; 60 1978; 30 1960; 38 2000; 41 1975 1992; 58 1999; 40 1972; 46 1995; 294 1996; 37 1994; 62 1998; 44 2001; 86 1993b; 208 1968; 12 1996a; 40 1980; 34 1995; 21 1994; 36 1994; 35 1975; 188 2000; 123 1977; 34 1992; 42 1998; 51 1992; 89 1996; 67 1998; 57 1993; 628 1990; 38 1967; 45 2000; 22 1994; 271 1997; 24 1997; 23 1995; 10 1999; 68 1989; 181 1996; 93 1995; 358 2002; 81 1975; 32 1999; 222 1989; 26 1991; 138 1996; 16 1983; 38 1976b; 26 1995; 5 1998; 22 1972; 26 1996b; 47 1979; 45 1993a; 60 1989; 10 1979; 47 2000; 39 1986; 126 1978; 87 2000; 426 1989; 164 1993; 54 1994; 14 1996; 40 1994; 16 1976a 1994; 3 1988; 318 1985; 150 1998; 8 e_1_2_31_12_1 e_1_2_31_35_1 e_1_2_31_58_1 e_1_2_31_10_1 e_1_2_31_37_1 e_1_2_31_79_1 e_1_2_31_39_1 e_1_2_31_80_1 Staley J. K. (e_1_2_31_64_1) 1994; 271 Thiessen B. (e_1_2_31_67_1) 1990; 38 e_1_2_31_61_1 McGeer E. (e_1_2_31_46_1) 1976 e_1_2_31_40_1 e_1_2_31_63_1 e_1_2_31_82_1 e_1_2_31_42_1 e_1_2_31_44_1 e_1_2_31_24_1 e_1_2_31_2_1 e_1_2_31_23_1 e_1_2_31_47_1 e_1_2_31_68_1 e_1_2_31_4_1 e_1_2_31_21_1 e_1_2_31_26_1 e_1_2_31_6_1 e_1_2_31_28_1 Hirai S. (e_1_2_31_29_1) 1968; 12 Frey K. A. (e_1_2_31_18_1) 2001; 86 Wilson J. M. (e_1_2_31_76_1) 1994; 14 Côté L. J. (e_1_2_31_8_1) 1983; 38 Volkow N. D. (e_1_2_31_73_1) 1996; 37 e_1_2_31_50_1 e_1_2_31_71_1 e_1_2_31_16_1 e_1_2_31_31_1 e_1_2_31_54_1 Staley J. K. (e_1_2_31_65_1) 1995; 21 e_1_2_31_77_1 e_1_2_31_14_1 e_1_2_31_33_1 e_1_2_31_56_1 e_1_2_31_75_1 e_1_2_31_11_1 e_1_2_31_36_1 Mozley P. D. (e_1_2_31_49_1) 1999; 40 e_1_2_31_57_1 e_1_2_31_38_1 e_1_2_31_59_1 Irwin I. (e_1_2_31_32_1) 1994; 3 DiChiara G. (e_1_2_31_9_1) 1995; 38 e_1_2_31_81_1 e_1_2_31_60_1 e_1_2_31_62_1 e_1_2_31_43_1 e_1_2_31_45_1 e_1_2_31_66_1 e_1_2_31_69_1 e_1_2_31_3_1 e_1_2_31_22_1 e_1_2_31_25_1 e_1_2_31_48_1 e_1_2_31_5_1 e_1_2_31_20_1 e_1_2_31_27_1 e_1_2_31_7_1 Pirker W. (e_1_2_31_52_1) 2000; 41 e_1_2_31_70_1 Lloyd K. G. (e_1_2_31_41_1) 1972; 26 e_1_2_31_19_1 e_1_2_31_74_1 e_1_2_31_17_1 e_1_2_31_30_1 e_1_2_31_51_1 e_1_2_31_72_1 e_1_2_31_15_1 e_1_2_31_53_1 e_1_2_31_78_1 e_1_2_31_13_1 e_1_2_31_34_1 e_1_2_31_55_1 |
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| Snippet | Because age‐related changes in brain dopaminergic innervation are assumed to influence human disorders involving dopamine (DA), we measured the levels of... Because age-related changes in brain dopaminergic innervation are assumed to influence human disorders involving dopamine (DA), we measured the levels of... |
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| SubjectTerms | Adolescent Adult Age Factors Aged Aged, 80 and over Aging - metabolism aromatic l‐amino acid decarboxylase Aromatic-L-Amino-Acid Decarboxylases - analysis Biological and medical sciences Biomarkers - analysis blot immunolabeling Child Child, Preschool Corpus Striatum - chemistry Development. Senescence. Regeneration. Transplantation Dopamine - analysis Dopamine Plasma Membrane Transport Proteins dopamine transporter Female Fundamental and applied biological sciences. Psychology Homovanillic Acid - analysis Humans Infant Infant, Newborn Male Membrane Glycoproteins - analysis Membrane Transport Proteins - analysis Middle Aged Nerve Tissue Proteins Neuropeptides Phosphopyruvate Hydratase - analysis postmortem Presynaptic Terminals - chemistry Presynaptic Terminals - metabolism Reference Values Tyrosine 3-Monooxygenase - analysis tyrosine hydroxylase Vertebrates: nervous system and sense organs Vesicular Biogenic Amine Transport Proteins Vesicular Monoamine Transport Proteins vesicular monoamine transporter 2 |
| Title | Marked disparity between age‐related changes in dopamine and other presynaptic dopaminergic markers in human striatum |
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