{"id":813,"date":"2016-09-08T14:53:53","date_gmt":"2016-09-08T12:53:53","guid":{"rendered":"http:\/\/www.scivit.de\/lang\/?p=813"},"modified":"2016-09-12T23:46:59","modified_gmt":"2016-09-12T21:46:59","slug":"is-there-hope-for-alzheimers-disease","status":"publish","type":"post","link":"https:\/\/www.scivit.de\/lang\/archive\/813","title":{"rendered":"Is there hope for Alzheimer’s disease?"},"content":{"rendered":"

[et_pb_section admin_label=“Sektion“ fullwidth=“on“ specialty=“off“][et_pb_fullwidth_image admin_label=“Volle Breite des Bildes“ src=“https:\/\/www.scivit.de\/lang\/wp-content\/uploads\/2016\/09\/PlaqueFinal.png“ alt=“Amyloid-beta plaques“ title_text=“Sharks“ show_in_lightbox=“off“ url_new_window=“off“ use_overlay=“off“ animation=“left“ use_border_color=“off“ border_color=“#ffffff“ border_style=“solid“] [\/et_pb_fullwidth_image][\/et_pb_section][et_pb_section admin_label=“section“][et_pb_row admin_label=“Zeile“][et_pb_column type=“4_4″][et_pb_post_title admin_label=“Posttitel“ title=“on“ meta=“on“ author=“on“ date=“on“ categories=“on“ comments=“on“ featured_image=“off“ featured_placement=“below“ parallax_effect=“on“ parallax_method=“on“ text_orientation=“left“ text_color=“dark“ text_background=“off“ text_bg_color=“rgba(255,255,255,0.9)“ module_bg_color=“rgba(255,255,255,0)“ title_all_caps=“off“ use_border_color=“off“ border_color=“#ffffff“ border_style=“solid“] [\/et_pb_post_title][\/et_pb_column][\/et_pb_row][et_pb_row admin_label=“row“][et_pb_column type=“4_4″][et_pb_text admin_label=“Summary“ background_layout=“light“ text_orientation=“left“ use_border_color=“off“ border_color=“#ffffff“ border_style=“solid“ text_font=“|on|||“ text_font_size=“18″]<\/p>\n

Alzheimer’s disease is a neurodegenerative affection, where the degeneration of neuronal tissue is accompanied by the wide-scale deposition of remnant material. Amyloid -beta plaques are prominent components of this material. It has been speculated for a long time that the deposition of such plaques might be the causal reason for neurodegeneration in the course of Alzheimer’s disease. Now scientists from Switzerland and the US succeeded in reducing the formation of Amyloid-beta plaques in mice and humans. The concomitant improvement of neurological symptoms strongly suggests that amyloid-beta plaques are at least in part responsible for the disease and that there is hope for therapeutic improvements.<\/span><\/p>\n

[\/et_pb_text][\/et_pb_column][\/et_pb_row][et_pb_row admin_label=“row“ make_fullwidth=“off“ use_custom_width=“off“ width_unit=“on“ use_custom_gutter=“off“ padding_mobile=“off“ allow_player_pause=“off“ parallax=“off“ parallax_method=“off“ make_equal=“off“ parallax_1=“off“ parallax_method_1=“off“ column_padding_mobile=“on“][et_pb_column type=“4_4″][et_pb_text admin_label=“Text“ background_layout=“light“ text_orientation=“left“ use_border_color=“off“ border_color=“#ffffff“ border_style=“solid“ text_font_size=“18″]<\/p>\n

Amyloid-beta plaques are produced from fragments of the amyloid precursor protein. This protein is produced in the nervous system and seems to play a role during formation of the brain. Under certain circumstances, including Alzheimer’s disease specific fragments of the protein are accumulating and aggregating as shown above (structure from Schuetz et al., taken from Pubmed Stucture: 2MVX). Sevigny et al. could now demonstrate that a specific antibody against the aggregated fragments reduces the amount of plaques in the brain (in mice and humans) and slows down development of dementia in human patients. <\/span><\/p>\n

Source: Sevigny et al., Nature doi:10.1038\/nature19323<\/a><\/p>\n

 <\/p>\n

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