[et_pb_section fb_built=”1″ _builder_version=”3.22.7″ custom_padding=”||5px|||”][et_pb_row _builder_version=”3.25″][et_pb_column type=”4_4″ _builder_version=”3.25″ custom_padding=”|||” custom_padding__hover=”|||”][et_pb_text _builder_version=”3.27.4″]<\/p>\n
[\/et_pb_text][\/et_pb_column][\/et_pb_row][\/et_pb_section][et_pb_section fb_built=”1″ specialty=”on” _builder_version=”3.22.3″ custom_padding=”24px|0px|25px|0px|false|false”][et_pb_column type=”3_4″ specialty_columns=”3″ _builder_version=”3.25″ custom_padding=”|||” custom_padding__hover=”|||”][et_pb_row_inner _builder_version=”3.25″][et_pb_column_inner saved_specialty_column_type=”3_4″ _builder_version=”3.25″ custom_padding=”|||” custom_padding__hover=”|||”][et_pb_blurb title=”Editoral in Hungarian ” url=”https:\/\/mppt.hu\/magazin\/pdf\/xvi-evfolyam-2-szam\/szerklevel_makkos.pdf” url_new_window=”on” image=”https:\/\/mppt.hu\/wp-content\/uploads\/2019\/04\/pdf.png” icon_placement=”left” image_max_width=”105%” content_max_width=”1100px” _builder_version=”3.22.7″ header_font=”||||||||” header_font_size=”17px” header_line_height=”1.3em” body_font=”||on||||||” body_line_height=”1.3em” link_option_url=”https:\/\/mppt.hu\/magazin\/pdf\/xvi-evfolyam-2-szam\/szerklevel_makkos.pdf” link_option_url_new_window=”on”]<\/p>\n
Zolt\u00e1n Makkos<\/p>\n
[\/et_pb_blurb][et_pb_toggle title=”Abstract” closed_toggle_text_color=”#000000″ closed_toggle_background_color=”rgba(0,0,0,0)” icon_color=”#0c71c3″ _builder_version=”3.22.7″ title_font=”|600|||||||” title_letter_spacing=”1px” text_orientation=”justified” custom_padding=”0px||10px” border_width_all=”0px” border_width_bottom=”1px”]<\/p>\n
A nyilv\u00e1nval\u00f3nak t\u0171n\u0151 v\u00e1laszon t\u00fal, ami m\u00f6g\u00f6tt az a k\u00f6nnyen \u00e9rthet\u0151 meg\u00e1llap\u00edt\u00e1s \u00e1ll, hogy ha pszich\u00f3zis, akkor antipszichotikum, \u00e9rdemes \u00e1tgondolni, hogy a mindennapi gyakorlatban milyen esetekben haszn\u00e1ljuk, milyen esetekben \u201ehisz\u00fcnk\u201d ezen szerek hat\u00e9konys\u00e1g\u00e1ban. T\u00e9ny, hogy az ebbe a gy\u00f3gyszercsal\u00e1dba tartoz\u00f3, egyes tulajdons\u00e1gaikban jelent\u0151sen k\u00fcl\u00f6nb\u00f6z\u0151 pszichofarmakonokkal \u00e9vtizedek \u00f3ta hat\u00e9konyan tudjuk gy\u00f3gy\u00edtani a betegeinket. A nagysz\u00e1m\u00fa j\u00f3 eredm\u00e9ny\u0171 kezel\u00e9s olyan betegcsoportokat is \u00e9rintett, illetve \u00e9rint, akik eset\u00e9ben t\u00fall\u00e9p\u00fcnk a klasszikus pszichotikus betegs\u00e9gek, \u00edgy a szkizofr\u00e9nia spektrum betegs\u00e9g \u00e9s a m\u00e1ni\u00e1s \u00e1llapottal j\u00e1r\u00f3 affekt\u00edv betegs\u00e9gek kateg\u00f3ri\u00e1j\u00e1n, mellyel k\u00f6nnyen off-label helyzetben tal\u00e1lhatjuk magunkat. A gy\u00f3gyszercsoport elnevez\u00e9se t\u00f6bb v\u00e1ltoz\u00e1son is \u00e1tesett, m\u00edg eljutottunk a jelenleg haszn\u00e1latos, hat\u00e1s-mell\u00e9khat\u00e1s profilon alapul\u00f3 els\u0151 gener\u00e1ci\u00f3s antipszichotikumok (FGA) \u00e9s m\u00e1sodik gener\u00e1ci\u00f3s antipszichotikumok (SGA) megjel\u00f6l\u00e9sig. Megjegyzend\u0151, hogy a gy\u00f3gyszert\u00f6rzsben az antipszichotikumok a pszicholeptikumok alcsoportjak\u00e9nt szerepelnek, \u00edgy a \u201elepszist\u0151l\u201d csak r\u00e9szben tudtunk megszabadulni.<\/p>\n
N\u00e9h\u00e1ny gondolatig id\u0151zz\u00fcnk a pszich\u00f3zis fogalm\u00e1n\u00e1l, ami \u201eellen\u201d adjuk ezeket a gy\u00f3gyszereket.\u00a0 A pszich\u00f3zis fogalma a XIX. sz\u00e1zadban jelent meg, s\u00falyos gondolkod\u00e1si-, \u00e9rzelmi- \u00e9s viselked\u00e9si zavart jel\u00f6l. Jellemz\u0151je az objekt\u00edv \u00e9s szubjekt\u00edv \u00e9lm\u00e9nyek megk\u00fcl\u00f6nb\u00f6ztet\u00e9s\u00e9nek zavara, vagyis a val\u00f3s\u00e1gvizsg\u00e1lat (realit\u00e1skontroll) el\u00e9gtelens\u00e9ge. Tudatzavar \u00e9ber tudat mellett. Fontos kiemelni, hogy elt\u00e9r\u0151 etiopatogenezis \u00e9s kimenetel jellemzi. A pszich\u00f3zis fogalm\u00e1t t\u00e1gabban is \u00e9rtelmezhetj\u00fck, gondoljunk az affekt\u00edv pszich\u00f3zisra, mely major depresszi\u00f3val jellemzett k\u00f3r\u00e1llapotokat jel\u00f6l, vagy a \u201epsychosis maniaco-depressiva\u201d-ra. Ezen t\u00falmen\u0151en az addikt\u00edv spektrum zavarokban \u00e9szlelhet\u0151 elvon\u00e1si- \u201etoxikus\u201d-, \u00e9s bel\u00e1t\u00e1si-probl\u00e9m\u00e1k, valamint az idegrendszer fejl\u0151d\u00e9si zavaraiban jelentkez\u0151 viselked\u00e9szavarok \u201eellen\u201d is alkalmazunk antipszichotikumokat bizonyos esetekben.<\/p>\n
Az antipszichotikumok alkalmaz\u00e1si el\u0151irataiban szerepl\u0151 ter\u00e1pi\u00e1s javallatok szerint ezen gy\u00f3gyszerek f\u0151 indik\u00e1ci\u00f3s ter\u00fclete a korszer\u0171 SGA-k eset\u00e9n ak\u00e1r\u00a0 kiz\u00e1r\u00f3lagosan a szkizofr\u00e9nia betegs\u00e9g, illetve a m\u00e1ni\u00e1s \u00e1llapottal jellemzett bipol\u00e1ris zavar. Bizonyos SGA szereket nemzetk\u00f6zi aj\u00e1nl\u00e1sok f\u00e1zisprofilaktikumk\u00e9nt is javasolnak. Az FGA-k eset\u00e9n a javallat b\u0151vebb, nemcsak a szorosabb \u00e9rtelemben vett pszich\u00f3zisokra is vonatkozik. Az elm\u00falt \u00e9vtizedek klinikai tapasztalatai alapj\u00e1n a szkizofr\u00e9nia spektrum betegs\u00e9gekben \u00e9szlelhet\u0151 pozit\u00edv t\u00fcnetek eset\u00e9n egy\u00e9rtelm\u0171 a sikeres kezel\u00e9s \u00e9s a negat\u00edv t\u00fcneteket illet\u0151en (az SGA szerekkel) is vannak j\u00f3 eredm\u00e9nyek. A hossz\u00fat\u00e1v\u00fa fenntart\u00f3 (p.o. vagy depot) antipszichotikum ter\u00e1pia bizony\u00edtottan relapszus-prevenci\u00f3s hat\u00e1s\u00fa, illetve kiemelend\u0151 a szuicid magatart\u00e1st cs\u00f6kkent\u0151 hat\u00e1s (clozapin). Azonban a kognit\u00edv-affekt\u00edv t\u00fcneti roml\u00e1st \u00e9s a betegs\u00e9g progresszi\u00f3j\u00e1t illet\u0151en, mely t\u00e9nyez\u0151k jelent\u0151sen meghat\u00e1rozz\u00e1k az \u00e9letmin\u0151s\u00e9get, a kezel\u00e9si hat\u00e9konys\u00e1g k\u00e9rd\u00e9ses \u00e9s nem kiel\u00e9g\u00edt\u0151.\u00a0<\/p>\n
Mindezek alapj\u00e1n mi ellen adjuk az antipszichotikumainkat?\u00a0 Winton-Brown \u00e9s mtsai (2014) a pszich\u00f3zis \u00e9s dopamin szab\u00e1lyoz\u00e1si zavar t\u00e9m\u00e1j\u00e1ban \u00edrt legfrissebb szakirodalmi \u00f6sszefoglal\u00f3 tanulm\u00e1nyukban r\u00e1mutatnak, hogy neurok\u00e9miai vizsg\u00e1latok \u00fajfent meger\u0151s\u00edtik a pszichotikus \u00e1llapotokban a szubkortik\u00e1lis-striat\u00e1lis r\u00e9gi\u00f3ban a dopaminanyagcsere-zavar jelenl\u00e9t\u00e9t. Elm\u00e9let\u00fck szerint a k\u00f3ros jelent\u0151s\u00e9gad\u00e1s a dopaminanyagcsere-zavaron kereszt\u00fcl vezet pszichotikus gondolkod\u00e1szavarhoz, pszich\u00f3zishoz. A funkcion\u00e1lis MRI vizsg\u00e1latok jelent\u0151s\u00e9gad\u00e1si feladatok eset\u00e9n a prefront\u00e1lis \u00e9s a striat\u00e1lis dopaminerg projekci\u00f3k ter\u00fcletein jeleznek v\u00e1ltoz\u00e1sokat. A pszich\u00f3zisokat jellemz\u0151 t\u00e9veszm\u00e9k kialakul\u00e1s\u00e1ban a mentaliz\u00e1ci\u00f3s folyamatok saj\u00e1ts\u00e1gai, az aberr\u00e1ns jelent\u0151s\u00e9gtulajdon\u00edt\u00e1s fokoz\u00f3d\u00e1sa igazolhat\u00f3 (Nagy H., K\u00e9ri Sz. \u00e9s mtsai, 2012)<\/p>\n
Sz\u00e1mos klinikai vizsg\u00e1lat elemzi az antipszichotikumok hat\u00e9konys\u00e1g\u00e1t major depresszi\u00f3ban. Ezen betegs\u00e9gben az a gondolkod\u00e1si be\u00e1ll\u00edt\u00f3d\u00e1s, mely minden k\u00fcls\u0151 ingernek negat\u00edv jelent\u00e9st ad illetve tulajdon\u00edt, arra utal, hogy a depresszi\u00f3 legal\u00e1bb annyira gondolkod\u00e1si zavar, mint hangulati probl\u00e9ma. Klinikai tapasztalat, hogy adott esetben pszichotikus szint\u0171 depresszi\u00f3s \u00e1llapot n\u00e9lk\u00fcl is sikeres lehet az antipszichotikummal v\u00e9gzett augment\u00e1ci\u00f3. Ha az eml\u00edtett elm\u00e9let igaz, magyar\u00e1zhat\u00f3v\u00e1 v\u00e1lnak a sikeres antipszichotikum kezel\u00e9sek az \u00e9rzelmileg labilis, pszichotikus dekompenz\u00e1ci\u00f3ra hajlamos, k\u00fcls\u0151 ingerekre adott maladapt\u00edv reakci\u00f3kkal jellemzett szem\u00e9lyis\u00e9gzavarok eset\u00e9n.<\/p>\n
Az idegrendszer fejl\u0151d\u00e9si zavaraihoz \u00e9s az organikus pszichoszindr\u00f3m\u00e1khoz t\u00e1rsul\u00f3 s\u00falyos viselked\u00e9szavarok eset\u00e9n az ingerekre adott adapt\u00e1ci\u00f3s funkci\u00f3k jelent\u0151sen s\u00e9r\u00fclnek, t\u00f6bb antipszichotikum javallat\u00e1ban szerepel ezen \u00e1llapotok kezel\u00e9se. K\u00f6z\u00f6s pont a vesz\u00e9ly\u00e9rzet meg\u00e9l\u00e9se, mely fesz\u00fclts\u00e9ghez, f\u00e9lelemhez vezet. Az id\u0151skorban jelentkez\u0151 agit\u00e1lts\u00e1g, pszich\u00f3zis eset\u00e9n az antipszichotikumokkal v\u00e9gzett ter\u00e1pi\u00e1kkal kapcsolatban szint\u00e9n nagysz\u00e1m\u00fa klinikai tapasztalat gy\u0171lt \u00f6ssze az elm\u00falt \u00e9vtizedekben. Els\u0151 gener\u00e1ci\u00f3s antipszichotikum (haloperidol, tiaprid) eset\u00e9n javallatk\u00e9nt is megjelenik, azonban valamennyi alkalmaz\u00e1si el\u0151irat, aj\u00e1nl\u00e1s figyelmeztet, hogy demencia betegs\u00e9g fenn\u00e1ll\u00e1sa eset\u00e9n (BPSD \u2013 behavioral and psychological symptoms of dementia) ker\u00fclend\u0151 az antipszichotikum alkalmaz\u00e1sa a megn\u00f6vekedett mortalit\u00e1si kock\u00e1zat miatt. Mindezeket figyelembe v\u00e9ve a ter\u00e1pi\u00e1ban marad\u00e1si vizsg\u00e1latokban ezen betegpopul\u00e1ci\u00f3 eredm\u00e9nyei is\u00a0 szerepelnek, az SGA-k k\u00f6z\u00fcl hat\u00e9konys\u00e1gban kiemelkedik a risperidon \u00e9s aripiprazol. Az USA-b\u00f3l sz\u00e1rmaz\u00f3 gy\u00f3gyszerfel\u00edr\u00e1si adatok alapj\u00e1n nagysz\u00e1m\u00fa \u201eoff-label\u201d antipszichotikum fel\u00edr\u00e1s t\u00f6rt\u00e9nik ezen a t\u00e9ren az eml\u00edtetteken k\u00edv\u00fcl az olanzapint \u00e9s quetiapint illet\u0151en is. Katharine Gammon a Medscape port\u00e1lon 2013-ban Arai \u00e9s mtsai. nagy elemsz\u00e1m\u00fa, prospekt\u00edv cohort vizsg\u00e1lat\u00e1r\u00f3l sz\u00e1molt be, ahol a kutat\u00f3k arra az eredm\u00e9nyre jutottak, hogy Alzheimer-betegs\u00e9g eset\u00e9n az antipszichotikumok alkalmaz\u00e1sa nem n\u00f6veli a mortalit\u00e1si kock\u00e1zatot.\u00a0<\/p>\n
A klinikai tapasztalatok \u00e9s a szakirodalom alapj\u00e1n sz\u00e1mos t\u00fcneti k\u00e9p eset\u00e9n alkalmazhat\u00f3k az antipszichotikumok, azonban a t\u00fal sz\u00e9lesk\u00f6r\u0171 alkalmaz\u00e1s, \u201ekipr\u00f3b\u00e1l\u00e1s\u201d a tudom\u00e1nyos megk\u00f6zel\u00edt\u00e9st\u0151l val\u00f3 elt\u00e1volod\u00e1st jelentene. A gy\u00f3gyszerekre alkalmazott \u201eanti,\u201d vagyis valaminek az ellenszere kifejez\u00e9s kedvelt elnevez\u00e9s az orvostudom\u00e1nyban, de tal\u00e1n ink\u00e1bb egyfajta modul\u00e1l\u00f3, harmoniz\u00e1l\u00f3, helyre\u00e1ll\u00edt\u00f3 szerep igazol\u00f3dik. A hat\u00e9konyabb \u00e9s biztons\u00e1gosabb kezel\u00e9sekhez nagysz\u00e1m\u00fa alap-, illetve klinikai kutat\u00e1s sz\u00fcks\u00e9ges a j\u00f6v\u0151ben.<\/p>\n<\/div>\n
[\/et_pb_toggle][et_pb_blurb title=”Application of pharmaco functional magnetic resonance imaging (phMRI) in the research of affective disorders” url=”https:\/\/mppt.hu\/magazin\/pdf\/xvi-evfolyam-2-szam\/edes.pdf” url_new_window=”on” image=”https:\/\/mppt.hu\/wp-content\/uploads\/2019\/04\/pdf.png” icon_placement=”left” image_max_width=”105%” content_max_width=”1100px” _builder_version=”3.22.7″ header_font=”||||||||” header_font_size=”17px” header_line_height=”1.3em” body_font=”||on||||||” body_line_height=”1.3em” link_option_url=”https:\/\/mppt.hu\/magazin\/pdf\/xvi-evfolyam-2-szam\/edes.pdf” link_option_url_new_window=”on”]<\/p>\n
Andrea Edit \u00c9des, X\u00e9nia Gonda, Gy\u00f6rgy Bagdy and Gabriella Juh\u00e1sz<\/p>\n
[\/et_pb_blurb][et_pb_toggle title=”Abstract” closed_toggle_text_color=”#000000″ closed_toggle_background_color=”rgba(0,0,0,0)” icon_color=”#0c71c3″ _builder_version=”3.22.7″ title_font=”|600|||||||” title_letter_spacing=”1px” text_orientation=”justified” custom_padding=”0px||10px” border_width_all=”0px” border_width_bottom=”1px”]<\/p>\n
Many common psychiatric disorders such as depression and anxiety disorders are associated with dysfunction in the monoamine neurotransmission in the central nervous system.
However, the investigation of these pathophysiological processes in the human living brain
is difficult. In case of functional magnetic resonance imaging (fMRI), a non-invasive method
for the examination of brain activity, the activity-inducing stimulus is generally a cognitive
psychological test, while during pharmacological magnetic resonance imaging (phMRI) the
activation is triggered by a specific pharmacon. In the present work we review the available
scientific literature related to this method using literature search in PubMed. Through application of a selective pharmacon like the selective serotonine reuptake inhibitors (SSRIs)
citalopram or escitalopram in a challenge phMRI study, the serotonergic neurotransmitter
system can be examined specifically, the functioning brain areas involved in its effect become
observable.. With modulation phMRI we can monitor the long-term effect of an antidepressant or we can examine the immediate effect of a single dose of the medication on congitive
psychological functions like emotional processing. Thus, the application of phMRI methods
may help deepen our understanding of serotonergic function in the living human brain as
well as of diseases related to serotonergic neurotransmitter system dysfunction.<\/p>\n
(Neuropsychopharmacol Hung 2014; 16(2): 59\u201366)<\/em><\/p>\n Keywords: functional magnetic resonance imaging, pharmacoMRI, depression, antidepressant treatment, emotion processing<\/p>\n<\/div>\n [\/et_pb_toggle][et_pb_blurb title=”The role of parkin in Parkinson\u2019s disease” url=”https:\/\/mppt.hu\/magazin\/pdf\/xvi-evfolyam-2-szam\/miklya_parkin.pdf” url_new_window=”on” image=”https:\/\/mppt.hu\/wp-content\/uploads\/2019\/04\/pdf.png” icon_placement=”left” image_max_width=”105%” content_max_width=”1100px” _builder_version=”3.22.7″ header_font=”||||||||” header_font_size=”17px” header_line_height=”1.3em” body_font=”||on||||||” body_line_height=”1.3em” link_option_url=”https:\/\/mppt.hu\/magazin\/pdf\/xvi-evfolyam-2-szam\/miklya_parkin.pdf” link_option_url_new_window=”on”]<\/p>\n Ildik\u00f3 Miklya, Patr\u00edcia G\u00f6ltl, Florencia\u00a0 Hafenscher and No\u00e9mi Pencz<\/p>\n [\/et_pb_blurb][et_pb_toggle title=”Abstract” closed_toggle_text_color=”#000000″ closed_toggle_background_color=”rgba(0,0,0,0)” icon_color=”#0c71c3″ _builder_version=”3.22.7″ title_font=”|600|||||||” title_letter_spacing=”1px” text_orientation=”justified” custom_padding=”0px||10px” border_width_all=”0px” border_width_bottom=”1px”]<\/p>\n Parkin (Parkinson juvenile disease protein 2) is a ~52 kDa (426 amino acid) enzyme protein, (Neuropsychopharmacol Hung 2014; 16(2): 67\u201376)<\/em><\/p>\n Keywords: parkin, Parkinson\u2019s disease, protein aggregation, mitochondrial dysfunction, mutation<\/p>\n<\/div>\n [\/et_pb_toggle][et_pb_blurb title=”The role of alpha-synuclein in Parkinson’s disease” url=”https:\/\/mppt.hu\/magazin\/pdf\/xvi-evfolyam-2-szam\/miklya_szinuklein.pdf” url_new_window=”on” image=”https:\/\/mppt.hu\/wp-content\/uploads\/2019\/04\/pdf.png” icon_placement=”left” image_max_width=”105%” content_max_width=”1100px” _builder_version=”3.22.7″ header_font=”||||||||” header_font_size=”17px” header_line_height=”1.3em” body_font=”||on||||||” body_line_height=”1.3em” link_option_url=”https:\/\/mppt.hu\/magazin\/pdf\/xvi-evfolyam-2-szam\/miklya_szinuklein.pdf” link_option_url_new_window=”on”]<\/p>\n Ildik\u00f3 Miklya, No\u00e9mi Pencz, Florencia\u00a0 Hafenscher and Patr\u00edcia G\u00f6ltl<\/p>\n [\/et_pb_blurb][et_pb_toggle title=”Abstract” closed_toggle_text_color=”#000000″ closed_toggle_background_color=”rgba(0,0,0,0)” icon_color=”#0c71c3″ _builder_version=”3.22.7″ title_font=”|600|||||||” title_letter_spacing=”1px” text_orientation=”justified” custom_padding=”0px||10px” border_width_all=”0px” border_width_bottom=”1px”]<\/p>\n \u03b1-synuclein, a small protein (140 amino acids) encoded by the SNCA gene is the best known (Neuropsychopharmacol Hung 2014; 16(2): 77\u201384)<\/em><\/p>\n Keywords: \u03b1-synuclein, conformational disease, neurodegenerative disease, Parkinson\u2019s disease, prion<\/p>\n<\/div>\n [\/et_pb_toggle][et_pb_blurb title=”Neurocognitive endophenotypes in psychiatric genetics” url=”https:\/\/mppt.hu\/magazin\/pdf\/xvi-evfolyam-2-szam\/kotyuk.pdf” url_new_window=”on” image=”https:\/\/mppt.hu\/wp-content\/uploads\/2019\/04\/pdf.png” icon_placement=”left” image_max_width=”105%” content_max_width=”1100px” _builder_version=”3.22.7″ header_font=”||||||||” header_font_size=”17px” header_line_height=”1.3em” body_font=”||on||||||” body_line_height=”1.3em” link_option_url=”https:\/\/mppt.hu\/magazin\/pdf\/xvi-evfolyam-2-szam\/kotyuk.pdf” link_option_url_new_window=”on”]<\/p>\n Eszter Kotyuk, M\u00e1ria\u00a0 Sasv\u00e1ri-Sz\u00e9kely and Anna Sz\u00e9kely<\/p>\n [\/et_pb_blurb][et_pb_toggle title=”Abstract” closed_toggle_text_color=”#000000″ closed_toggle_background_color=”rgba(0,0,0,0)” icon_color=”#0c71c3″ _builder_version=”4.6.6″ title_font=”|600|||||||” title_letter_spacing=”1px” text_orientation=”justified” custom_padding=”0px||10px” border_width_all=”0px” border_width_bottom=”1px”]<\/p>\n Psychiatric genetics aims to map genetic factors of psychiatric disorders with complex inheritance. The most commonly used phenotype is the categorical variable of the presence (Neuropsychopharmacol Hung 2014; 16(2): 85\u201390)<\/em><\/p>\n Keywords: psychiatric genetics, genetic association studies, neurocognitive endophenotype<\/p>\n<\/div>\n [\/et_pb_toggle][et_pb_blurb title=”The influence of attention-deficit hyperactivity disorder on quality of life: case reports” url=”https:\/\/mppt.hu\/magazin\/pdf\/xvi-evfolyam-2-szam\/dallos.pdf” url_new_window=”on” image=”https:\/\/mppt.hu\/wp-content\/uploads\/2019\/04\/pdf.png” icon_placement=”left” image_max_width=”105%” content_max_width=”1100px” _builder_version=”3.22.7″ header_font=”||||||||” header_font_size=”17px” header_line_height=”1.3em” body_font=”||on||||||” body_line_height=”1.3em” link_option_url=”https:\/\/mppt.hu\/magazin\/pdf\/xvi-evfolyam-2-szam\/dallos.pdf” link_option_url_new_window=”on”]<\/p>\n Gy\u00f6ngyv\u00e9r Dallos and Judit Bal\u00e1zs<\/p>\n [\/et_pb_blurb][et_pb_toggle title=”Abstract” closed_toggle_text_color=”#000000″ closed_toggle_background_color=”rgba(0,0,0,0)” icon_color=”#0c71c3″ _builder_version=”4.6.6″ title_font=”|600|||||||” title_letter_spacing=”1px” text_orientation=”justified” custom_padding=”0px||10px” border_width_all=”0px” border_width_bottom=”1px”]<\/p>\n Recently the concept of Quality of Life has gained increasing importance in Psychiatry. Studies focusing on how much attention-deficit hyperactivity disorder (ADHD) \u2013 one of the most (Neuropsychopharmacol Hung 2014; 16(2): 91\u201397)<\/em><\/p>\n <\/em><\/p>\n Keywords: Quality of Life, QoL, attention-deficit hyperactivity disorder, ADHD<\/p>\n<\/div>\n [\/et_pb_toggle][\/et_pb_column_inner][\/et_pb_row_inner][\/et_pb_column][et_pb_column type=”1_4″ _builder_version=”3.25″ custom_padding=”|||” custom_padding__hover=”|||”][et_pb_image src=”https:\/\/mppt.hu\/wp-content\/uploads\/2019\/05\/b1-2014-juni_kicsi2.jpg” align_tablet=”center” align_phone=”” align_last_edited=”on|desktop” _builder_version=”3.23″ box_shadow_style=”preset3″][\/et_pb_image][\/et_pb_column][\/et_pb_section]<\/p>\n","protected":false},"excerpt":{"rendered":" VOLUME 16, ISSUE 2, JUNE 2014Zolt\u00e1n MakkosL\u00e9teznek-e antipszichotikumok? Makkos Zolt\u00e1n A nyilv\u00e1nval\u00f3nak t\u0171n\u0151 v\u00e1laszon t\u00fal, ami m\u00f6g\u00f6tt az a k\u00f6nnyen \u00e9rthet\u0151 meg\u00e1llap\u00edt\u00e1s \u00e1ll, hogy ha pszich\u00f3zis, akkor antipszichotikum, \u00e9rdemes \u00e1tgondolni, hogy a mindennapi gyakorlatban milyen esetekben haszn\u00e1ljuk, milyen esetekben \u201ehisz\u00fcnk\u201d ezen szerek hat\u00e9konys\u00e1g\u00e1ban. T\u00e9ny, hogy az ebbe a gy\u00f3gyszercsal\u00e1dba tartoz\u00f3, egyes tulajdons\u00e1gaikban jelent\u0151sen k\u00fcl\u00f6nb\u00f6z\u0151 pszichofarmakonokkal […]<\/p>\n","protected":false},"author":4,"featured_media":48309,"comment_status":"closed","ping_status":"closed","template":"","meta":{"_et_pb_use_builder":"on","_et_pb_old_content":"","_et_gb_content_width":"","footnotes":""},"project_category":[61],"project_tag":[],"class_list":["post-49318","project","type-project","status-publish","has-post-thumbnail","hentry","project_category-2014-en"],"_links":{"self":[{"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/project\/49318","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/project"}],"about":[{"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/types\/project"}],"author":[{"embeddable":true,"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/users\/4"}],"replies":[{"embeddable":true,"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/comments?post=49318"}],"version-history":[{"count":8,"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/project\/49318\/revisions"}],"predecessor-version":[{"id":49585,"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/project\/49318\/revisions\/49585"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/media\/48309"}],"wp:attachment":[{"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/media?parent=49318"}],"wp:term":[{"taxonomy":"project_category","embeddable":true,"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/project_category?post=49318"},{"taxonomy":"project_tag","embeddable":true,"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/project_tag?post=49318"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}
encoded by PARK2 gene and located on the 6q chromosome. It plays an important role in the
ubiquitin-proteasome system and acts as a regulator of protein breakdown. Parkin is located in
the cytoplasma until a sustained depolarization occurs as a result of which it is translocated to
the mitochondrial surface and induces the degradation of various membrane proteins which
are candidates for mitophagia. Parkin is essential for cellular mitochondrial integrity. Parkin
mutation leads to the accumulation of missfolded, aggregated proteins and degenerated
mitochondria. The role of these changes in the pathomechanism of neurodegenerative diseases is well-known. It was a general belief for a long time that Parkinson\u2019s disease is without
genetic component a sporadic disease. In 1997 a point mutation was, however, discovered
in the \u03b1-synuclein gene, which caused dominantly inherited parkinsonism. At least 10 other
genes were thereafter detected the mutation or deletion of which cause monogenic parkinsonism. Parkin mutation is responsible for about 50% of familial cases and for 10 to 20% of
youth cases. According to the present views the improper regulation of protein aggregation and a dysfunction of the ubiquitin-proteasome system may be the common pathway
of sporadic and hereditary Parkinson\u2019s disease. In the future it might have therapeutic value
that parkin has versatile neuroprotective activity (against \u03b1-synuclein toxicity, proteasomal
dysfunction, oxidative stress, kainite-induced and dopamine-mediated toxicity) as a result
of which any reduction of parkin level or activity may cause damage in neuronal integrity.<\/p>\n
isoform of the synuclein protein family. Though its physiological role is still not fully clarified, there is growing experimental evidence for a causal role of \u03b1-synuclein in the so-called
conformational-neurodegenerative diseases. Conformational changes in the structure of
the native soluble protein form insoluble neurotoxic aggregates and finally contribute to
the formation of inclusion Lewy-bodies and Lewy-neurites. Neurodegeneration first hits the
olfactory system, the peripheral autonomic nervous system, the enteric nervous system and
the dorsal vagal motoneurons. The middle stage of the disease hits the dopaminergic neurons
of the substantia nigra; and the neocortex is affected only in the late stage of the disease.
This precise order of neurodegeneration is not always valid, but increases the likelihood that
Lewy-bodies and neurodegenaration spread to intact areas in a prion-like way. Prions are
infectious proteins which do not contain nucleic acids and cause diseases because they form
toxic aggregates and filaments by misfolding in a \u03b2-sheet-rich conformation. The misfolded
protein behaves like a template inducing conformational change in the wild type proteins
causing cross-reaction and leading to neurodegeneration. Later, the defective proteins may
infect healthy nerve cells, thus neurodegeneration is extended. Growing experimental evidence shows that monomers and aggregates of \u03b1-synuclein are secreted via exocytosis from
damaged nerve cells and taken up via endocytosis by healthy nerve cells furnishing evidence
for the prion-like role of \u03b1-synuclein.<\/p>\n
or absence of a disease (case-control model). However, the biological background of various
psychiatric disease categories often overlaps. Thus, the use of endophenotypes based on
specific biological mechanisms seems to be a more efficient approach in genetic association
studies. Results confirm that categorical variables as phenotypes are statistically not so sensitive
in identification of a genetic association as well-chosen endophenotypes. Current literature
advocates a growing significance of analyzing dimensional neurocognitive endophenotypes
in genetic association studies, as well as in developing diagnostic category systems with biological backgrounds.<\/p>\n
prevalent psychiatric disorders among children \u2013 affects the every day life found that children
with ADHD had significantly lower Quality of Life than healthy controls or children with other
psychiatric or physical disorders. In the current paper we present the case of two boys with
ADHD and their families. These cases demonstrate that adequate treatment of the symptoms
of ADHD can improve Quality of Life of the patients and their families, moreover, different life
events can worsen the symptoms of ADHD. Professionals should ensure flexible treatment,
which conforms to the above described processes.<\/p>\n