Aging-associated neuropathology in Werner syndrome
Abstract Werner syndrome (WS) is an autosomal recessive disorder associated with evidence of accelerated systemic aging, but generally thought not to involve the central nervous system. We examined two WS cases utilizing a sensitive Bielschowsky silver stain and immunohistochemistry for amyloid β pe...
Ausführliche Beschreibung
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Englisch |
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1998 |
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4 |
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Springer Online Journal Archives 1860-2002 |
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in: Acta neuropathologica - 1961, 96(1998) vom: Apr., Seite 421-424 |
Übergeordnetes Werk: |
volume:96 ; year:1998 ; month:04 ; pages:421-424 ; extent:4 |
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520 | |a Abstract Werner syndrome (WS) is an autosomal recessive disorder associated with evidence of accelerated systemic aging, but generally thought not to involve the central nervous system. We examined two WS cases utilizing a sensitive Bielschowsky silver stain and immunohistochemistry for amyloid β peptide (Aβ) and hyperphosphorylated tau. Extensive frontal and temporal lobe Aβ deposition was observed in the oldest (age 57 years) WS case and restricted neurofibrillary pathology was seen in the medial temporal lobe of both cases. The severity of Aβ deposition in the medial temporal lobe of the oldest case exceeded that observed in our control cases and that reported in the literature. Our findings suggest that the apparent accelerated aging observed in WS can involve the central nervous system and may implicate the recently observed WRN locus mutation associated with WS in the neuropathology of aging and aging-associated diseases. | ||
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(DE-627)NLEJ203622960 DE-627 ger DE-627 rakwb eng Aging-associated neuropathology in Werner syndrome 1998 4 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Werner syndrome (WS) is an autosomal recessive disorder associated with evidence of accelerated systemic aging, but generally thought not to involve the central nervous system. We examined two WS cases utilizing a sensitive Bielschowsky silver stain and immunohistochemistry for amyloid β peptide (Aβ) and hyperphosphorylated tau. Extensive frontal and temporal lobe Aβ deposition was observed in the oldest (age 57 years) WS case and restricted neurofibrillary pathology was seen in the medial temporal lobe of both cases. The severity of Aβ deposition in the medial temporal lobe of the oldest case exceeded that observed in our control cases and that reported in the literature. Our findings suggest that the apparent accelerated aging observed in WS can involve the central nervous system and may implicate the recently observed WRN locus mutation associated with WS in the neuropathology of aging and aging-associated diseases. Springer Online Journal Archives 1860-2002 Leverenz, J. B. oth Yu, Chang-En oth Schellenberg, Gerard D. oth in Acta neuropathologica 1961 96(1998) vom: Apr., Seite 421-424 (DE-627)NLEJ188990917 (DE-600)1458410-4 1432-0533 nnns volume:96 year:1998 month:04 pages:421-424 extent:4 http://dx.doi.org/10.1007/s004010050914 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 96 1998 4 421-424 4 |
spelling |
(DE-627)NLEJ203622960 DE-627 ger DE-627 rakwb eng Aging-associated neuropathology in Werner syndrome 1998 4 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Werner syndrome (WS) is an autosomal recessive disorder associated with evidence of accelerated systemic aging, but generally thought not to involve the central nervous system. We examined two WS cases utilizing a sensitive Bielschowsky silver stain and immunohistochemistry for amyloid β peptide (Aβ) and hyperphosphorylated tau. Extensive frontal and temporal lobe Aβ deposition was observed in the oldest (age 57 years) WS case and restricted neurofibrillary pathology was seen in the medial temporal lobe of both cases. The severity of Aβ deposition in the medial temporal lobe of the oldest case exceeded that observed in our control cases and that reported in the literature. Our findings suggest that the apparent accelerated aging observed in WS can involve the central nervous system and may implicate the recently observed WRN locus mutation associated with WS in the neuropathology of aging and aging-associated diseases. Springer Online Journal Archives 1860-2002 Leverenz, J. B. oth Yu, Chang-En oth Schellenberg, Gerard D. oth in Acta neuropathologica 1961 96(1998) vom: Apr., Seite 421-424 (DE-627)NLEJ188990917 (DE-600)1458410-4 1432-0533 nnns volume:96 year:1998 month:04 pages:421-424 extent:4 http://dx.doi.org/10.1007/s004010050914 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 96 1998 4 421-424 4 |
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(DE-627)NLEJ203622960 DE-627 ger DE-627 rakwb eng Aging-associated neuropathology in Werner syndrome 1998 4 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Werner syndrome (WS) is an autosomal recessive disorder associated with evidence of accelerated systemic aging, but generally thought not to involve the central nervous system. We examined two WS cases utilizing a sensitive Bielschowsky silver stain and immunohistochemistry for amyloid β peptide (Aβ) and hyperphosphorylated tau. Extensive frontal and temporal lobe Aβ deposition was observed in the oldest (age 57 years) WS case and restricted neurofibrillary pathology was seen in the medial temporal lobe of both cases. The severity of Aβ deposition in the medial temporal lobe of the oldest case exceeded that observed in our control cases and that reported in the literature. Our findings suggest that the apparent accelerated aging observed in WS can involve the central nervous system and may implicate the recently observed WRN locus mutation associated with WS in the neuropathology of aging and aging-associated diseases. Springer Online Journal Archives 1860-2002 Leverenz, J. B. oth Yu, Chang-En oth Schellenberg, Gerard D. oth in Acta neuropathologica 1961 96(1998) vom: Apr., Seite 421-424 (DE-627)NLEJ188990917 (DE-600)1458410-4 1432-0533 nnns volume:96 year:1998 month:04 pages:421-424 extent:4 http://dx.doi.org/10.1007/s004010050914 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 96 1998 4 421-424 4 |
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(DE-627)NLEJ203622960 DE-627 ger DE-627 rakwb eng Aging-associated neuropathology in Werner syndrome 1998 4 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Werner syndrome (WS) is an autosomal recessive disorder associated with evidence of accelerated systemic aging, but generally thought not to involve the central nervous system. We examined two WS cases utilizing a sensitive Bielschowsky silver stain and immunohistochemistry for amyloid β peptide (Aβ) and hyperphosphorylated tau. Extensive frontal and temporal lobe Aβ deposition was observed in the oldest (age 57 years) WS case and restricted neurofibrillary pathology was seen in the medial temporal lobe of both cases. The severity of Aβ deposition in the medial temporal lobe of the oldest case exceeded that observed in our control cases and that reported in the literature. Our findings suggest that the apparent accelerated aging observed in WS can involve the central nervous system and may implicate the recently observed WRN locus mutation associated with WS in the neuropathology of aging and aging-associated diseases. Springer Online Journal Archives 1860-2002 Leverenz, J. B. oth Yu, Chang-En oth Schellenberg, Gerard D. oth in Acta neuropathologica 1961 96(1998) vom: Apr., Seite 421-424 (DE-627)NLEJ188990917 (DE-600)1458410-4 1432-0533 nnns volume:96 year:1998 month:04 pages:421-424 extent:4 http://dx.doi.org/10.1007/s004010050914 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 96 1998 4 421-424 4 |
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(DE-627)NLEJ203622960 DE-627 ger DE-627 rakwb eng Aging-associated neuropathology in Werner syndrome 1998 4 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Werner syndrome (WS) is an autosomal recessive disorder associated with evidence of accelerated systemic aging, but generally thought not to involve the central nervous system. We examined two WS cases utilizing a sensitive Bielschowsky silver stain and immunohistochemistry for amyloid β peptide (Aβ) and hyperphosphorylated tau. Extensive frontal and temporal lobe Aβ deposition was observed in the oldest (age 57 years) WS case and restricted neurofibrillary pathology was seen in the medial temporal lobe of both cases. The severity of Aβ deposition in the medial temporal lobe of the oldest case exceeded that observed in our control cases and that reported in the literature. Our findings suggest that the apparent accelerated aging observed in WS can involve the central nervous system and may implicate the recently observed WRN locus mutation associated with WS in the neuropathology of aging and aging-associated diseases. Springer Online Journal Archives 1860-2002 Leverenz, J. B. oth Yu, Chang-En oth Schellenberg, Gerard D. oth in Acta neuropathologica 1961 96(1998) vom: Apr., Seite 421-424 (DE-627)NLEJ188990917 (DE-600)1458410-4 1432-0533 nnns volume:96 year:1998 month:04 pages:421-424 extent:4 http://dx.doi.org/10.1007/s004010050914 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 96 1998 4 421-424 4 |
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Abstract Werner syndrome (WS) is an autosomal recessive disorder associated with evidence of accelerated systemic aging, but generally thought not to involve the central nervous system. We examined two WS cases utilizing a sensitive Bielschowsky silver stain and immunohistochemistry for amyloid β peptide (Aβ) and hyperphosphorylated tau. Extensive frontal and temporal lobe Aβ deposition was observed in the oldest (age 57 years) WS case and restricted neurofibrillary pathology was seen in the medial temporal lobe of both cases. The severity of Aβ deposition in the medial temporal lobe of the oldest case exceeded that observed in our control cases and that reported in the literature. Our findings suggest that the apparent accelerated aging observed in WS can involve the central nervous system and may implicate the recently observed WRN locus mutation associated with WS in the neuropathology of aging and aging-associated diseases. |
abstractGer |
Abstract Werner syndrome (WS) is an autosomal recessive disorder associated with evidence of accelerated systemic aging, but generally thought not to involve the central nervous system. We examined two WS cases utilizing a sensitive Bielschowsky silver stain and immunohistochemistry for amyloid β peptide (Aβ) and hyperphosphorylated tau. Extensive frontal and temporal lobe Aβ deposition was observed in the oldest (age 57 years) WS case and restricted neurofibrillary pathology was seen in the medial temporal lobe of both cases. The severity of Aβ deposition in the medial temporal lobe of the oldest case exceeded that observed in our control cases and that reported in the literature. Our findings suggest that the apparent accelerated aging observed in WS can involve the central nervous system and may implicate the recently observed WRN locus mutation associated with WS in the neuropathology of aging and aging-associated diseases. |
abstract_unstemmed |
Abstract Werner syndrome (WS) is an autosomal recessive disorder associated with evidence of accelerated systemic aging, but generally thought not to involve the central nervous system. We examined two WS cases utilizing a sensitive Bielschowsky silver stain and immunohistochemistry for amyloid β peptide (Aβ) and hyperphosphorylated tau. Extensive frontal and temporal lobe Aβ deposition was observed in the oldest (age 57 years) WS case and restricted neurofibrillary pathology was seen in the medial temporal lobe of both cases. The severity of Aβ deposition in the medial temporal lobe of the oldest case exceeded that observed in our control cases and that reported in the literature. Our findings suggest that the apparent accelerated aging observed in WS can involve the central nervous system and may implicate the recently observed WRN locus mutation associated with WS in the neuropathology of aging and aging-associated diseases. |
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