{"id":49333,"date":"2010-09-29T09:53:14","date_gmt":"2010-09-29T09:53:14","guid":{"rendered":"https:\/\/mppt.hu\/project\/2010-szeptember-xii-evfolyam-3-szam\/"},"modified":"2020-10-29T16:07:06","modified_gmt":"2020-10-29T16:07:06","slug":"2010-szeptember-xii-evfolyam-3-szam","status":"publish","type":"project","link":"https:\/\/mppt.hu\/en\/project\/2010-szeptember-xii-evfolyam-3-szam\/","title":{"rendered":"Volume 12, Issue 3, September 2010"},"content":{"rendered":"

[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

Volume 12, Issue 3, September 2010<\/h4>\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\/xii-evfolyam-3-szam\/szerk_level_web_20101018.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\/xii-evfolyam-3-szam\/szerk_level_web_20101018.pdf” link_option_url_new_window=”on”]<\/p>\n

Ildik\u00f3 Miklya<\/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

Amikor az a megtiszteltet\u00e9s \u00e9rt, hogy a Neuropsychopharmacologia Hungarica szerkeszt\u0151bizotts\u00e1g\u00e1nak tagj\u00e1v\u00e1 v\u00e1lasztottak, \u00e9s az ilyenkor szok\u00e1sos bek\u00f6sz\u00f6nt\u0151 lev\u00e9l tartalm\u00e1n gondolkodtam, eszembe jutott, milyen hat\u00e1st gyakorolt r\u00e1m Ban, Healy, \u00e9s Shorter \u2019The Rise of Psychopharmacology\u2019 c\u00edm\u0171 k\u00f6tete. Ez a jubileumi kiadv\u00e1ny, melyet a Collegium Internationale Neuropsychopharmacologicum (CINP) megsz\u00fclet\u00e9s\u00e9nek 50. \u00e9vfordul\u00f3j\u00e1ra megeml\u00e9kez\u00e9sk\u00e9nt adtak ki, ragyog\u00f3 \u00f6sszefoglal\u00e1sa annak a forradalomnak, mely az 1950-es \u00e9vekben kezd\u0151d\u00f6tt el, majd teljesedett ki a neuropszichofarmakol\u00f3gia l\u00e9legzetel\u00e1ll\u00edt\u00f3 fejl\u0151d\u00e9se eredm\u00e9nyek\u00e9nt. Olyan \u00faj hat\u00e1sm\u00f3d\u00fa vegy\u00fcletcsal\u00e1dokat dolgoztak ki gyors egym\u00e1sut\u00e1nban, melyek lehet\u0151v\u00e9 tett\u00e9k a pszich\u00e9s m\u0171k\u00f6d\u00e9seket alapvet\u0151en befoly\u00e1sol\u00f3 \u00e9lettani mechanizmusok molekul\u00e1ris alapjainak megismer\u00e9s\u00e9t. Az \u00faj ismeretek lehet\u0151v\u00e9 tett\u00e9k az elmebetegs\u00e9gek eladdig elk\u00e9pzelhetetlen hat\u00e9konys\u00e1g\u00fa gy\u00f3gyszeres befoly\u00e1sol\u00e1s\u00e1t.\u00a0
\u00a0\u00a0\u00a0\u00a0 \u00c9s most egy \u00fajabb forradalom kezd\u0151dik el. A 21. sz\u00e1zad a nanovil\u00e1g felt\u00e1r\u00e1s\u00e1nak, sz\u00e9lesk\u00f6r\u0171 megismer\u00e9s\u00e9nek \u00e9s a nanotechnol\u00f3gi\u00e1nak az \u00e9vsz\u00e1zada lesz \u2013 vallj\u00e1k sokan. Ez a k\u00fcsz\u00f6b\u00f6n \u00e1ll\u00f3 nanoforradalom igaz\u00e1b\u00f3l a term\u00e9szet aj\u00e1nd\u00e9ka, hiszen a 4 milli\u00e1rd \u00e9ves f\u00f6ldi \u00e9let a kezdetekt\u0151l \u00fagy fejl\u0151d\u00f6tt, hogy az \u00e9l\u0151 szervezetek az atto\/femto\/piko\/nano molekul\u00e1ris szinten \u00e9p\u00edtkezve fejlesztett\u00e9k ki legfontosabb \u00e9lettani mechanizmusaikat, melyek molekul\u00e1ris szint\u0171 megval\u00f3s\u00edt\u00e1s\u00e1t most kezdi a tudom\u00e1ny felt\u00e1rni. Ez a technol\u00f3gia, a term\u00e9szet e \u201elego j\u00e1t\u00e9ka\u201d eredm\u00e9nyezi az \u00e9l\u0151 vil\u00e1g v\u00e9gtelen vari\u00e1ci\u00f3j\u00e1t. Szerencs\u00e9re a tudom\u00e1ny \u00e9s a technika eljutott arra a fejletts\u00e9gi szintre, hogy a 10-9 m\u00e9teres nanotartom\u00e1nyban is tud m\u00e1r c\u00e9lzottan \u00e9p\u00edtkezni.
\u00a0\u00a0\u00a0\u00a0 A nanomedicina ter\u00fclet\u00e9re szor\u00edtkozva a nanotechnol\u00f3gia min\u0151s\u00e9gi ugr\u00e1st jelenthet a megl\u00e9v\u0151 gy\u00f3gyszerek hat\u00e9konyabb\u00e1 t\u00e9tel\u00e9ben \u00e9s mell\u00e9khat\u00e1saik cs\u00f6kkent\u00e9s\u00e9ben az\u00e1ltal, hogy ir\u00e1ny\u00edthat\u00f3v\u00e1 v\u00e1lnak a molekul\u00e1k \u00e9s csak az optim\u00e1lis hat\u00e1s j\u00f6n l\u00e9tre. A multifunkcion\u00e1lis nanogy\u00f3gyszer c\u00e9lba juttat\u00f3 komponense p\u00e9ld\u00e1ul biztos\u00edtja, hogy a hat\u00f3anyag a specifikus molekul\u00e1ris kamp\u00f3 seg\u00edts\u00e9g\u00e9vel csak a beteg sejthez k\u00f6t\u0151dj\u00f6n. Vagy az emberis\u00e9g gy\u00f3gyszerkincse kib\u0151v\u00fclhet olyan \u00faj anyagokkal, amelyek hat\u00e9konys\u00e1ga m\u00e1r a nanosk\u00e1l\u00e1n is kimutathat\u00f3, \u00e9s elhagyhatjuk a milligrammos, mikrogrammos m\u00e9rettartom\u00e1nyokat, ami \u00faj elm\u00e9letek megsz\u00fclet\u00e9s\u00e9re \u00e9s a prevenci\u00f3s ter\u00e1pia kialakul\u00e1s\u00e1ra ad v\u00e9gtelen lehet\u0151s\u00e9get.
\u00a0\u00a0\u00a0\u00a0 J\u00f3 p\u00e9lda erre a Knoll nev\u00e9hez f\u0171z\u0151d\u0151 agyt\u00f6rzsi enhancer regul\u00e1ci\u00f3 felfedez\u00e9se, melyet a deprenil \u00e9s\u00a0 a BPAP kidolgoz\u00e1sa tett lehet\u0151v\u00e9. Az agyt\u00f6rzsi enhancer regul\u00e1ci\u00f3 olyan enhancer\u00e9rz\u00e9keny neuronok l\u00e9t\u00e9n alapul, melyek ingerl\u00e9kenys\u00e9g\u00fcket endog\u00e9n, vagy szintetikus enhancer vegy\u00fcletek (pl.: PEA, triptamin, illetve ezek szintetikus anal\u00f3gjai, (-)-deprenil, (-)-BPAP) hat\u00e1s\u00e1ra a m\u00e1sodperc t\u00f6rt r\u00e9sze alatt m\u00e1r femto-pikomolekul\u00e1ris koncentr\u00e1ci\u00f3ban fokozni k\u00e9pesek. \u00c9ppen ez\u00e9rt \u00edg\u00e9retes prevent\u00edv c\u00e9l\u00fa alkalmaz\u00e1suk. Mivel az enhancer hat\u00e1s pontos mechanizmusa m\u00e9g nem ismert, a nanomedicina \u00faj megk\u00f6zel\u00edt\u00e9si technik\u00e1inak figyelembev\u00e9tel\u00e9vel a liposz\u00f3m\u00e1ba z\u00e1rt igen kis mennyis\u00e9g\u0171 hat\u00f3anyaghoz kapcsolt jelad\u00f3 biztos\u00edthatn\u00e1 az eddig ismeretlen folyamat nyomon k\u00f6vet\u00e9s\u00e9t, meghat\u00e1roz\u00e1s\u00e1t.\u00a0
\u00a0\u00a0\u00a0\u00a0 A nanoter\u00e1pia ma m\u00e9g csak a tumoros \u00e9s gomb\u00e1s megbeteged\u00e9sek eset\u00e9ben alkalmaz nanokapszul\u00e1kat, de a nanomedicina minden bizonnyal egyre nagyobb szerepet kap az orvostudom\u00e1ny t\u00f6bbi ter\u00fclet\u00e9n is, nem hagyva ki a pszichi\u00e1tri\u00e1t, neurol\u00f3gi\u00e1t \u00e9s geri\u00e1tri\u00e1t sem, \u00faj rem\u00e9nyeket keltve a pszichi\u00e1triai \u00e9s a neurodegenerat\u00edv betegs\u00e9gek, valamint az \u00f6reged\u00e9s kezel\u00e9s\u00e9ben.\u00a0<\/div>\n

[\/et_pb_toggle][et_pb_blurb title=”The feasibility of synthetic enhancer substances for preventive nanotherapy” url=”https:\/\/mppt.hu\/magazin\/pdf\/xii-evfolyam-3-szam\/miklyaweb_20101018.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\/xii-evfolyam-3-szam\/miklyaweb_20101018.pdf” link_option_url_new_window=”on”]<\/p>\n

Ildik\u00f3 Miklya<\/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

\n

Nanotechnology, the great promise of the 21st century, may revolutionize also the art
of healing. Previously unexpected broadening of diagnostic procedures and methods
to deliver specific drugs acting in lower than nanomolecular concentrations right to the
target cells may play a crucial role in the rapid development of preventive medicine.
In this context, (-)-deprenyl\/selegiline, a drug developed 40 years ago and still worldwide used to treat Parkinson\u2019s disease, Alzheimer\u2019s disease and depression, by enhancing
the activity of catecholaminergic neurons in the brain stem via a previously unknown
mechanism [catecholaminergic activity enhancer (CAE) effect], is a highly promising
experimental tool for further research in this direction. The same fits for (-)-BPAP, the
newly developed enhancer substance, 100 times more potent than (-)-deprenyl, which in
contrast to the latter is not only an enhancer of the catecholaminergic neurons but also
of the serotonergic neurons in the brain stem. Tiny amounts of enhancer substances are
closed in liposomes and marked with a specific signal to help identify the exact location
of the target cells, through the activation of which the drug exerts its specific enhancer
effect. The method also offers an approach to better understand the up-to-the-present
unknown mechanism of the enhancer effect.<\/p>\n

Keywords<\/strong>: enhancer substances, enhancer regulation, (-)-deprenyl\/selegiline,
(-)-BPAP, nanotherapy<\/p>\n<\/div>\n

[\/et_pb_toggle][et_pb_blurb title=”The dopamin D3 receptor \u2013 the gray eminence of pharmacotherapy?” url=”https:\/\/mppt.hu\/magazin\/pdf\/xii-evfolyam-3-szam\/sumegi_dopamin_d3_web_2101018.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\/xii-evfolyam-3-szam\/sumegi_dopamin_d3_web_2101018.pdf” link_option_url_new_window=”on”]<\/p>\n

Andr\u00e1s S\u00fcmegi, \u00c9va Varga<\/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

\n

The dopamine system plays a crucial role in the pathophysiology of many neuropsychiatric
disorders. Altough there is sufficient information and knowledge about several dopamine
receptor subtypes and their functions, until the last decade the role of the D3
receptor was
almost unclear. Recent research data proved that the D3
receptor might have a significant
role in fine tuning the modulation of dopaminergic neurotransmission. Cariprazine is a
novel agent developed in Hungary, its activity on the dopamine D3
receptor might open
up new dimensions in the pharmacotherapy of schizophrenia and affective disorders.<\/p>\n

Keywords<\/strong>: dopamine system, dopamine, D3 receptor, cariprazine<\/p>\n<\/div>\n

[\/et_pb_toggle][et_pb_blurb title=”Long-term neuronal damage and recovery after a single dose of MDMA: expression and distribution of serotonin transporter in the rat brain” url=”https:\/\/mppt.hu\/magazin\/pdf\/xii-evfolyam-3-szam\/kirilly_web_20101018.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\/xii-evfolyam-3-szam\/kirilly_web_20101018.pdf” link_option_url_new_window=”on”]<\/p>\n

Eszter Kirilly<\/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

\n

\u201cEcstasy\u201d, 3,4-methylenedioxymethamphetamine (MDMA), an amphetamine analogue is one of the most widely used recreational drugs. In spite of the fact that neurotoxic effects of MDMA has been found in several species from rodents to non-human primates, and results increasingly point to damage also in human MDMA users, data about the sensitivity of different brain areas and the recovery after neuronal damage are scarce. Serotonin transporter (5-HTT) mRNA in the raphe nuclei also has not been examined. Humans with genetic predisposition for the slow metabolism of MDMA, the so-called \u201cpoor metabolizers\u201d of debrisoquin are at higher risk. Five- 9% of the Caucasian population is considered to carry this phenotype. These studies were carried out in Dark Agouti rats, a special strain that show decreased microsomal CYP2D1 isoenzyme activity, and thus may serve as a model of vulnerable human users. These works were designed to characterize MDMA-induced damage and recovery of the serotonergic system including sleep and morphological changes within 180 days. In our experiments we investigated the 5-HTT mRNA expression in the brainstem and medullary raphe nuclei, 5-HTT immunoreactive (IR) fibre densities in several brain areas, and 16 functional measures of sleep in response to a single dose of +\/- MDMA (15mgkg). Furthermore, behavioural experiments were performed 21 days after MDMA treatment. We found similar changes in 5-HTT mRNA expression in the examined raphe nuclei, namely transient increases 7 days after MDMA treatment followed by transient decreases at 21 days. Significant (20\u201340%), widespread reductions in 5-HTT-IR fibre density were detected in most brain areas at 7 and 21 days after MDMA administration. All cortical, but only some brainstem areas were damaged. Parallel to the neuronal damage we observed significant reductions in rapid eye movement (REM) sleep latency, increased fragmentation of sleep and increases in delta power spectra in non-REM sleep. At 180 days almost all functional changes in sleep were normalized together with 5-HTT mRNA expression in the examined raphe nuclei and the recovery of 5-HTT-IR fibre density in most brain areas. Our results also suggest that the acute MDMA administration abolished aggressive behaviour but MDMA pretreatment and the consequent depletion of serotonergic terminals did not affect aggression. Our findings concerning the changes detected in 5-HTT mRNA expression and fibre density indicate lasting impairment of the serotonergic system and suggest that a single use of MDMA may be associated with long-lasting cognitive, learning, memory and mood deficits and sleep disturbances particularly when a constellation of genetic vulnerability and certain environmental factors are present. Our data provide further evidence for the connection between altered serotonergic functions and sleep disturbance.<\/p>\n

Keywords:<\/strong>\u00a0MDMA, serotonin transporter, raphe nucleus, REM latency, aggression<\/p>\n<\/div>\n

[\/et_pb_toggle][et_pb_blurb title=”9-hydroxy-risperidone (9OHRIS) prevents stress-induced \u00df-actin overexpression in rat hippocampus” url=”https:\/\/mppt.hu\/magazin\/pdf\/xii-evfolyam-3-szam\/kalman_web_20101018.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\/xii-evfolyam-3-szam\/kalman_web_20101018.pdf” link_option_url_new_window=”on”]<\/p>\n

S\u00e1ra\u00a0<\/sup>K\u00e1lm\u00e1n, Magdolna\u00a0<\/sup>P\u00e1k\u00e1ski, Szabina\u00a0<\/sup>Sz\u0171cs, J\u00e1nos ifj.\u00a0<\/sup>K\u00e1lm\u00e1n , \u00d6rsike\u00a0<\/sup>Fazekas, Petra\u00a0<\/sup>S\u00e1ntha, Gyula\u00a0<\/sup>Szab\u00f3, Zolt\u00e1n\u00a0<\/sup>Janka and J\u00e1nos\u00a0<\/sup>K\u00e1lm\u00e1n<\/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

\n

Alzheimer\u2019s disease (AD) is the most frequent form of neurodegenerative dementias.
The aetiology and the exact pathomechanism of AD is not known, but stress has been
considered recently in the aetiology. Beside the abnormal metabolism of the amyloid
\u2013 precursor protein (APP), the hyperactivity of the mitogen \u2013 activated protein kinase 1
(MAPK1) involved in the hyperphosphorylation of the tau proteins \u2013 which are considered
as the major component of neurofibrillary tangles \u2013, in addition to \u00df-actin, being involved
in synaptogenesis and neuronal plasticity, are all considered as important contributors of
the development of AD specific neuropathological changes. The major aim of our present
investigation was to examine the effect of stress on the expression of APP, MAPK1 and
\u00df-actin mRNAs in the rat hippocampus and cortex. The effect of 9-hydroxy-risperidone
(9OHRIS) on the transcription of these genes was also examined. Adult, male Wistar rats
were exposed to chronic immobilization stress for 3 weeks. The 9OHRIS (4 mg\/bwkg)
was administred by gastric tube. Four groups were formed depending on the treatment:
(1) control, (2) stress, (3) 9OHRIS, (4) stress and parallel 9OHRIS treatment (n=5-6). The
expression of APP, MAPK1, \u00df-actin mRNAs from the perfused brain samples was measured
with real-time PCR technique. The \u00df-actin mRNA was significantly overexpressed in the
hippocampus after 3 weeks of stress treatment. On the other hand, the stress induced
hippocampal \u00df-actin mRNA overexpression was repressed by the 9OHRIS treatment.
There were no changes in the cortical or hippocampal expression of APP and MAPK1
mRNAs after neither the stress nor the 9OHRIS treatments. These results emphasize
the importance of the stress induced \u00df-actin expression in rat hippocampus. The stress
induced alterations in the \u00df-actin RNA expression could be associated with neuronal
plasticity and adaptional processes, which could be modified by the 9OHRIS treatment.
Our findings indicate that a second generation antipsychotic drug could have a beneficial
effect in the pathomechanism of stress and this may have relevance in the treatment of
such devastating conditions like AD and psychotic disorders.<\/p>\n

Keywords<\/strong>: Alzheimer\u2019s disease, stress, hippocampus, amyloid-precursor protein,
mitogen-activated protein kinase, \u00df-actin, 9-hydroxy-risperidone, real-time PCR<\/p>\n<\/div>\n

[\/et_pb_toggle][et_pb_blurb title=”Application of lamotrigine in bipolar disorder \u2013 3T MR spectroscopy follow up (part 1)” url=”https:\/\/mppt.hu\/magazin\/pdf\/xii-evfolyam-3-szam\/sumegi_esettan_web_20101018.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\/xii-evfolyam-3-szam\/sumegi_esettan_web_20101018.pdf” link_option_url_new_window=”on”]<\/p>\n

Andr\u00e1s\u00a0<\/sup>S\u00fcmegi, Szabolcs Hal\u00e1sz and Edit\u00a0<\/sup>Kliment<\/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

\n

MR spectroscopy (MRS) is a widely used and useful additional tool in the diagnostic
process of several neuropsychiatric disorders. Despite several MRS studies in bipolar
spectrum reserach, establishing a clean image about special metabolite alterations in
the disorder still needs further investigation. The first part of this case study presents a
bipolar II patient and her first 3T MR spectroscopy in drug-naive conditions, comparing
to a healthy subject. Having finished the first MRS investigation, we applied lamotrigine
medication. The ongoing second part of the study will show the data of the second MRS
scan, after 5 month of lamotrigine therapy.<\/p>\n

Kewyords<\/strong>: MR spectroscopy, bipolar disorder, N-Acetyl-Aspartate, cholin, creatin<\/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\/mppt_cimlap_20101018.jpg” align_tablet=”center” 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 12, Issue 3, September 2010Ildik\u00f3 MiklyaAmikor az a megtiszteltet\u00e9s \u00e9rt, hogy a Neuropsychopharmacologia Hungarica szerkeszt\u0151bizotts\u00e1g\u00e1nak tagj\u00e1v\u00e1 v\u00e1lasztottak, \u00e9s az ilyenkor szok\u00e1sos bek\u00f6sz\u00f6nt\u0151 lev\u00e9l tartalm\u00e1n gondolkodtam, eszembe jutott, milyen hat\u00e1st gyakorolt r\u00e1m Ban, Healy, \u00e9s Shorter \u2019The Rise of Psychopharmacology\u2019 c\u00edm\u0171 k\u00f6tete. Ez a jubileumi kiadv\u00e1ny, melyet a Collegium Internationale Neuropsychopharmacologicum (CINP) megsz\u00fclet\u00e9s\u00e9nek 50. \u00e9vfordul\u00f3j\u00e1ra […]<\/p>\n","protected":false},"author":4,"featured_media":48326,"comment_status":"closed","ping_status":"closed","template":"","meta":{"_et_pb_use_builder":"on","_et_pb_old_content":"","_et_gb_content_width":"","footnotes":""},"project_category":[65],"project_tag":[],"class_list":["post-49333","project","type-project","status-publish","has-post-thumbnail","hentry","project_category-2010-en"],"_links":{"self":[{"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/project\/49333","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=49333"}],"version-history":[{"count":4,"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/project\/49333\/revisions"}],"predecessor-version":[{"id":49713,"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/project\/49333\/revisions\/49713"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/media\/48326"}],"wp:attachment":[{"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/media?parent=49333"}],"wp:term":[{"taxonomy":"project_category","embeddable":true,"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/project_category?post=49333"},{"taxonomy":"project_tag","embeddable":true,"href":"https:\/\/mppt.hu\/en\/wp-json\/wp\/v2\/project_tag?post=49333"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}