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Matches in Nanopublications for { ?s ?p "[These findings suggest that (1) LB pathology can influence the clinical features of familial AD, (2) the E184D mutation of presenilin-1 may be associated with the LB formation through Abeta overproduction, although the process of LB formation is strongly affected by other unknown mechanisms, (3) in neurodegenerative disorders with LBs, there is a common pathophysiological background inducing NAC accumulation in neuritic plaques and astrocytes, and (4) the NAC accumulation in neuritic plaques is modulated by the abnormally aggregated tau protein.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine."@en ?g. }

• NP810204.RAW9J1F3vHGClI-78KZz2Ko7Cin7r_BmNKuHSpXc687mM130_assertion description "[These findings suggest that (1) LB pathology can influence the clinical features of familial AD, (2) the E184D mutation of presenilin-1 may be associated with the LB formation through Abeta overproduction, although the process of LB formation is strongly affected by other unknown mechanisms, (3) in neurodegenerative disorders with LBs, there is a common pathophysiological background inducing NAC accumulation in neuritic plaques and astrocytes, and (4) the NAC accumulation in neuritic plaques is modulated by the abnormally aggregated tau protein.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP810204.RAW9J1F3vHGClI-78KZz2Ko7Cin7r_BmNKuHSpXc687mM130_provenance.
• NP831668.RAes9Zbm7dHz2HH1BdpZ4rKVUavV1FFn-1i-KwMi9q8Dg130_assertion description "[These findings suggest that (1) LB pathology can influence the clinical features of familial AD, (2) the E184D mutation of presenilin-1 may be associated with the LB formation through Abeta overproduction, although the process of LB formation is strongly affected by other unknown mechanisms, (3) in neurodegenerative disorders with LBs, there is a common pathophysiological background inducing NAC accumulation in neuritic plaques and astrocytes, and (4) the NAC accumulation in neuritic plaques is modulated by the abnormally aggregated tau protein.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP831668.RAes9Zbm7dHz2HH1BdpZ4rKVUavV1FFn-1i-KwMi9q8Dg130_provenance.
• NP927637.RAp4L1-bIOTKlYsciZjSNMiH_nyBIuCLmhcOZl_K-PHZ0130_assertion description "[These findings suggest that (1) LB pathology can influence the clinical features of familial AD, (2) the E184D mutation of presenilin-1 may be associated with the LB formation through Abeta overproduction, although the process of LB formation is strongly affected by other unknown mechanisms, (3) in neurodegenerative disorders with LBs, there is a common pathophysiological background inducing NAC accumulation in neuritic plaques and astrocytes, and (4) the NAC accumulation in neuritic plaques is modulated by the abnormally aggregated tau protein.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP927637.RAp4L1-bIOTKlYsciZjSNMiH_nyBIuCLmhcOZl_K-PHZ0130_provenance.
• NP281714.RAw2xO_8WUrvB6QmwsK1D3OSdq_S7nWlyQ2vk1-9EnXA4130_assertion description "[These findings suggest that (1) LB pathology can influence the clinical features of familial AD, (2) the E184D mutation of presenilin-1 may be associated with the LB formation through Abeta overproduction, although the process of LB formation is strongly affected by other unknown mechanisms, (3) in neurodegenerative disorders with LBs, there is a common pathophysiological background inducing NAC accumulation in neuritic plaques and astrocytes, and (4) the NAC accumulation in neuritic plaques is modulated by the abnormally aggregated tau protein.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP281714.RAw2xO_8WUrvB6QmwsK1D3OSdq_S7nWlyQ2vk1-9EnXA4130_provenance.
• NP498935.RAgRw_o6XM5WKkuUAeXMaSVFd-Msd421ANwB57UaK21ag130_assertion description "[These findings suggest that (1) LB pathology can influence the clinical features of familial AD, (2) the E184D mutation of presenilin-1 may be associated with the LB formation through Abeta overproduction, although the process of LB formation is strongly affected by other unknown mechanisms, (3) in neurodegenerative disorders with LBs, there is a common pathophysiological background inducing NAC accumulation in neuritic plaques and astrocytes, and (4) the NAC accumulation in neuritic plaques is modulated by the abnormally aggregated tau protein.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP498935.RAgRw_o6XM5WKkuUAeXMaSVFd-Msd421ANwB57UaK21ag130_provenance.
• NP562130.RAhmkErb_SkZutWepeegS5HJOcVpk6YrwRTgpWO2ZeQ88130_assertion description "[These findings suggest that (1) LB pathology can influence the clinical features of familial AD, (2) the E184D mutation of presenilin-1 may be associated with the LB formation through Abeta overproduction, although the process of LB formation is strongly affected by other unknown mechanisms, (3) in neurodegenerative disorders with LBs, there is a common pathophysiological background inducing NAC accumulation in neuritic plaques and astrocytes, and (4) the NAC accumulation in neuritic plaques is modulated by the abnormally aggregated tau protein.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP562130.RAhmkErb_SkZutWepeegS5HJOcVpk6YrwRTgpWO2ZeQ88130_provenance.
• NP339841.RA0Ro5Df4QbDfkGOLdAt6PAwHRByeoGL3ifvKYA1vw2Vg130_assertion description "[These findings suggest that (1) LB pathology can influence the clinical features of familial AD, (2) the E184D mutation of presenilin-1 may be associated with the LB formation through Abeta overproduction, although the process of LB formation is strongly affected by other unknown mechanisms, (3) in neurodegenerative disorders with LBs, there is a common pathophysiological background inducing NAC accumulation in neuritic plaques and astrocytes, and (4) the NAC accumulation in neuritic plaques is modulated by the abnormally aggregated tau protein.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP339841.RA0Ro5Df4QbDfkGOLdAt6PAwHRByeoGL3ifvKYA1vw2Vg130_provenance.
• NP420337.RA5-k4E2nOz6JXZufYMfBw-aMB4ScQNLTbClFGRBG4D1g130_assertion description "[These findings suggest that (1) LB pathology can influence the clinical features of familial AD, (2) the E184D mutation of presenilin-1 may be associated with the LB formation through Abeta overproduction, although the process of LB formation is strongly affected by other unknown mechanisms, (3) in neurodegenerative disorders with LBs, there is a common pathophysiological background inducing NAC accumulation in neuritic plaques and astrocytes, and (4) the NAC accumulation in neuritic plaques is modulated by the abnormally aggregated tau protein.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP420337.RA5-k4E2nOz6JXZufYMfBw-aMB4ScQNLTbClFGRBG4D1g130_provenance.
• assertion description "[These findings suggest that (1) LB pathology can influence the clinical features of familial AD, (2) the E184D mutation of presenilin-1 may be associated with the LB formation through Abeta overproduction, although the process of LB formation is strongly affected by other unknown mechanisms, (3) in neurodegenerative disorders with LBs, there is a common pathophysiological background inducing NAC accumulation in neuritic plaques and astrocytes, and (4) the NAC accumulation in neuritic plaques is modulated by the abnormally aggregated tau protein.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." provenance.
• assertion description "[These findings suggest that (1) LB pathology can influence the clinical features of familial AD, (2) the E184D mutation of presenilin-1 may be associated with the LB formation through Abeta overproduction, although the process of LB formation is strongly affected by other unknown mechanisms, (3) in neurodegenerative disorders with LBs, there is a common pathophysiological background inducing NAC accumulation in neuritic plaques and astrocytes, and (4) the NAC accumulation in neuritic plaques is modulated by the abnormally aggregated tau protein.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." provenance.
• assertion description "[These findings suggest that (1) LB pathology can influence the clinical features of familial AD, (2) the E184D mutation of presenilin-1 may be associated with the LB formation through Abeta overproduction, although the process of LB formation is strongly affected by other unknown mechanisms, (3) in neurodegenerative disorders with LBs, there is a common pathophysiological background inducing NAC accumulation in neuritic plaques and astrocytes, and (4) the NAC accumulation in neuritic plaques is modulated by the abnormally aggregated tau protein.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." provenance.
• assertion description "[These findings suggest that (1) LB pathology can influence the clinical features of familial AD, (2) the E184D mutation of presenilin-1 may be associated with the LB formation through Abeta overproduction, although the process of LB formation is strongly affected by other unknown mechanisms, (3) in neurodegenerative disorders with LBs, there is a common pathophysiological background inducing NAC accumulation in neuritic plaques and astrocytes, and (4) the NAC accumulation in neuritic plaques is modulated by the abnormally aggregated tau protein.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." provenance.
• assertion description "[These findings suggest that (1) LB pathology can influence the clinical features of familial AD, (2) the E184D mutation of presenilin-1 may be associated with the LB formation through Abeta overproduction, although the process of LB formation is strongly affected by other unknown mechanisms, (3) in neurodegenerative disorders with LBs, there is a common pathophysiological background inducing NAC accumulation in neuritic plaques and astrocytes, and (4) the NAC accumulation in neuritic plaques is modulated by the abnormally aggregated tau protein.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." provenance.
• NP373129.RAQxJ2JwGv7Q7hB7lHR-e0SVMKDjRYfNUNzNgnlvvCXCQ130_assertion description "[These findings suggest that (1) LB pathology can influence the clinical features of familial AD, (2) the E184D mutation of presenilin-1 may be associated with the LB formation through Abeta overproduction, although the process of LB formation is strongly affected by other unknown mechanisms, (3) in neurodegenerative disorders with LBs, there is a common pathophysiological background inducing NAC accumulation in neuritic plaques and astrocytes, and (4) the NAC accumulation in neuritic plaques is modulated by the abnormally aggregated tau protein.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP373129.RAQxJ2JwGv7Q7hB7lHR-e0SVMKDjRYfNUNzNgnlvvCXCQ130_provenance.
• NP650803.RApaiNX74wwc_DNvvjCLmheoc4vKROuLO299S0xxJoRs4130_assertion description "[These findings suggest that (1) LB pathology can influence the clinical features of familial AD, (2) the E184D mutation of presenilin-1 may be associated with the LB formation through Abeta overproduction, although the process of LB formation is strongly affected by other unknown mechanisms, (3) in neurodegenerative disorders with LBs, there is a common pathophysiological background inducing NAC accumulation in neuritic plaques and astrocytes, and (4) the NAC accumulation in neuritic plaques is modulated by the abnormally aggregated tau protein.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP650803.RApaiNX74wwc_DNvvjCLmheoc4vKROuLO299S0xxJoRs4130_provenance.
• NP373128.RAhbgwa75uiXhtwkA1IWgecYT4KrBESCOXfAAlWxd9YsY130_assertion description "[These findings suggest that (1) LB pathology can influence the clinical features of familial AD, (2) the E184D mutation of presenilin-1 may be associated with the LB formation through Abeta overproduction, although the process of LB formation is strongly affected by other unknown mechanisms, (3) in neurodegenerative disorders with LBs, there is a common pathophysiological background inducing NAC accumulation in neuritic plaques and astrocytes, and (4) the NAC accumulation in neuritic plaques is modulated by the abnormally aggregated tau protein.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP373128.RAhbgwa75uiXhtwkA1IWgecYT4KrBESCOXfAAlWxd9YsY130_provenance.
• NP373131.RAtO00s9XYfxg4UaTrMxi02GQDrIn__4kfDmUvZnO9FmU130_assertion description "[These findings suggest that (1) LB pathology can influence the clinical features of familial AD, (2) the E184D mutation of presenilin-1 may be associated with the LB formation through Abeta overproduction, although the process of LB formation is strongly affected by other unknown mechanisms, (3) in neurodegenerative disorders with LBs, there is a common pathophysiological background inducing NAC accumulation in neuritic plaques and astrocytes, and (4) the NAC accumulation in neuritic plaques is modulated by the abnormally aggregated tau protein.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP373131.RAtO00s9XYfxg4UaTrMxi02GQDrIn__4kfDmUvZnO9FmU130_provenance.
• NP373130.RA9trhMzxes-7bAR5ScgjTGGQG_eoJNfPW5F1PuDXNvq8130_assertion description "[These findings suggest that (1) LB pathology can influence the clinical features of familial AD, (2) the E184D mutation of presenilin-1 may be associated with the LB formation through Abeta overproduction, although the process of LB formation is strongly affected by other unknown mechanisms, (3) in neurodegenerative disorders with LBs, there is a common pathophysiological background inducing NAC accumulation in neuritic plaques and astrocytes, and (4) the NAC accumulation in neuritic plaques is modulated by the abnormally aggregated tau protein.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP373130.RA9trhMzxes-7bAR5ScgjTGGQG_eoJNfPW5F1PuDXNvq8130_provenance.