المؤلفون: Kac, Przemysław R, González-Ortiz, Fernando, Emeršič, Andreja, Dulewicz, Maciej, Koutarapu, Srinivas, Turton, Michael, An, Yang, Smirnov, Denis, Kulczyńska-Przybik, Agnieszka, Varma, Vijay R, Ashton, Nicholas J, Montoliu-Gaya, Laia, Camporesi, Elena, Winkel, Izabela, Paradowski, Bogusław, Moghekar, Abhay, Troncoso, Juan C, Lashley, Tammaryn, Brinkmalm, Gunnar, Resnick, Susan M, Mroczko, Barbara, Kvartsberg, Hlin, Gregorič Kramberger, Milica, Hanrieder, Jörg, Čučnik, Saša, Harrison, Peter, Zetterberg, Henrik, Lewczuk, Piotr, Thambisetty, Madhav, Rot, Uroš, Galasko, Douglas, Blennow, Kaj, Karikari, Thomas K

المصدر: Nature Communications , 15 (1) , Article 2615. (2024)

مصطلحات موضوعية: Alzheimer's disease, Diagnostic markers

الوصف: Blood phosphorylated tau (p-tau) biomarkers, including p-tau217, show high associations with Alzheimer's disease (AD) neuropathologic change and clinical stage. Certain plasma p-tau217 assays recognize tau forms phosphorylated additionally at threonine-212, but the contribution of p-tau212 alone to AD is unknown. We developed a blood-based immunoassay that is specific to p-tau212 without cross-reactivity to p-tau217. Here, we examined the diagnostic utility of plasma p-tau212. In five cohorts (n = 388 participants), plasma p-tau212 showed high performances for AD diagnosis and for the detection of both amyloid and tau pathology, including at autopsy as well as in memory clinic populations. The diagnostic accuracy and fold changes of plasma p-tau212 were similar to those for p-tau217 but higher than p-tau181 and p-tau231. Immunofluorescent staining of brain tissue slices showed prominent p-tau212 reactivity in neurofibrillary tangles that co-localized with p-tau217 and p-tau202/205. These findings support plasma p-tau212 as a peripherally accessible biomarker of AD pathophysiology.

وصف الملف: text

العلاقة: https://discovery.ucl.ac.uk/id/eprint/10190310/1/s41467-024-46876-7.pdfTest; https://discovery.ucl.ac.uk/id/eprint/10190310Test/

الإتاحة: https://discovery.ucl.ac.uk/id/eprint/10190310/1/s41467-024-46876-7.pdfTest
https://discovery.ucl.ac.uk/id/eprint/10190310Test/

المؤلفون: Wężyk, Michalina, Berdyński, Mariusz, Figarski, Adam, Skrzypczak, Magdalena, Ginalski, Krzysztof, Zboch, Marzena, Winkel, Izabela, Żekanowski, Cezary

المصدر: International Journal of Molecular Sciences; Dec2023, Vol. 24 Issue 23, p16999, 28p

مصطلحات موضوعية: ALZHEIMER'S disease, GENE expression, CELL cycle regulation, CYCLIN-dependent kinases, GENETIC mutation, CELL cycle

مستخلص: Presenilin 1 (PS1) forms, via its large cytosolic loop, a trimeric complex with N-cadherin and β-catenin, which is a key component of Wnt signaling. PS1 undergoes phosphorylation at 353 and 357 serines upon enhanced activity and elevated levels of the GSK3β isoform. PS1 mutations surrounding these serines may alter the stability of the β-catenin complex. Such mutations are found in some cases of familial early-onset Alzheimer's disease (fEOAD), but their functional impact remains obscure. One of such variants of PS1, the A360T substitution, is located close to GSK3β-targeted serine residues. This variant was recently demonstrated in the French population, but more detail is needed to understand its biological effects. To assess the significance of this variant, we employed functional studies using a fibroblast cell line from an Alzheimer's disease case (a female proband) carrying the A360T mutation. Based on functional transcriptomic, cellular, and biochemical assays, we demonstrated atypically impaired β-catenin/GSK3β signaling in the A360T patient's fibroblasts. In detail, this was characterized by a decreased level of active cytosolic β-catenin and bound by PS1, an increased level of nuclear β-catenin, an increased level of inhibited GSK3β phosphorylated on Ser9, and enhanced interaction of GSK3β(Ser9) with PS1. Based on the transcriptomic profile of the A360T fibroblasts, we proposed a dysregulated transcriptional activity of β-catenin, exemplified by increased expression of various cyclin-dependent kinases and cyclins, such as cyclin D1, potentially inducing neurons' cell cycle re-entry followed by apoptosis. The A360T cells did not exhibit significant amyloid pathology. Therefore, cell death in this PS1 cytosolic loop mutation may be attributed to impaired β-catenin/GSK3β signaling rather than amyloid deposition per se. We further estimated the biological and clinical relevance of the A360T variant by whole exome sequencing (WES). WES was performed on DNA from the blood of an A360T female proband, as well as an unrelated male patient carrying the A360T mutation and his mutation-free daughter (both unavailable for the derivation of the fibroblast cell lines). WES confirmed the highest-priority AD causality of the A360T variant in PS1 and also profiled the pathways and processes involved in the A360T case, highlighting the greatest importance of altered Wnt signaling. [ABSTRACT FROM AUTHOR]

: Copyright of International Journal of Molecular Sciences is the property of MDPI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Doroszkiewicz, Julia, Farhan, Jakub Ali, Mroczko, Jan, Winkel, Izabela, Perkowski, Maciej, Mroczko, Barbara

المصدر: International Journal of Molecular Sciences; Nov2023, Vol. 24 Issue 21, p15721, 26p

مصطلحات موضوعية: TRACE metals, ALZHEIMER'S disease, PARKINSON'S disease, LEAD, ZINC, HEAVY metals, IRON

مستخلص: Trace elements and metals play critical roles in the normal functioning of the central nervous system (CNS), and their dysregulation has been implicated in neurodegenerative disorders such as Alzheimer's disease (AD) and Parkinson's disease (PD). In a healthy CNS, zinc, copper, iron, and manganese play vital roles as enzyme cofactors, supporting neurotransmission, cellular metabolism, and antioxidant defense. Imbalances in these trace elements can lead to oxidative stress, protein aggregation, and mitochondrial dysfunction, thereby contributing to neurodegeneration. In AD, copper and zinc imbalances are associated with amyloid-beta and tau pathology, impacting cognitive function. PD involves the disruption of iron and manganese levels, leading to oxidative damage and neuronal loss. Toxic metals, like lead and cadmium, impair synaptic transmission and exacerbate neuroinflammation, impacting CNS health. The role of aluminum in AD neurofibrillary tangle formation has also been noted. Understanding the roles of these elements in CNS health and disease might offer potential therapeutic targets for neurodegenerative disorders. The Codex Alimentarius standards concerning the mentioned metals in foods may be one of the key legal contributions to safeguarding public health. Further research is needed to fully comprehend these complex mechanisms and develop effective interventions. [ABSTRACT FROM AUTHOR]

: Copyright of International Journal of Molecular Sciences is the property of MDPI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Winkel, Izabela, Ermann, Natalia, Żelwetro, Agnieszka, Sambor, Bożydar, Mroczko, Barbara, Kornhuber, Johannes, Paradowski, Bogusław, Lewczuk, Piotr

مصطلحات موضوعية: ddc:610

الوصف: Extrapyramidal symptoms (EP) are not uncommon in Alzheimer’s Disease (AD); when present, they negatively influence the course of the disorder. A large proportion of AD patients shows concomitant Lewy bodies’ pathology post mortem. Total α Synuclein (αSyn) concentrations are frequently increased in the cerebrospinal fluid (CSF) of AD patients, but are decreased in Parkinson’s Disease (PD) and Dementia with Lewy Bodies (DLB). αSyn CSF concentrations in AD patients with EP (EP+) have not been reported so far. αSyn and the four Neurochemical Dementia Diagnostics (NDD) CSF biomarkers, (Aβ1-42, Aβ42/40, Tau, and pTau181), interpreted according to the Erlangen Score algorithm, were measured in patients with positive NDD results and presence of extrapyramidal symptoms (NDD + / EP+; n = 26), in patients with positive NDD results and absence of extrapyramidal symptoms (NDD+ / EP−; n = 54), and in subjects with negative NDD results (NDD−; n = 34). Compared to the NDD− controls (379.8 ± 125.2 pg/mL), NDD+ patients showed, on average, highly significantly increased CSF αSyn (519 ± 141.3 pg/mL, p < 0.01), but without differences between NDD+ / EP+ and NDD+ / EP− subgroups (p = 0. 38). Moderate but highly significant association was observed between concentrations of αSyn and Tau (r = 0.47, p < 0.01) and pTau181 (r = 0.65, p < 0.01). Adjusted for diagnoses, age, and sex, subjects with more advanced neurodegeneration on neuroimaging showed significantly lower αSyn concentrations (p < 0.02). In the setting AD versus controls, the area under the receiver operating characteristic (ROC) curve was 0.804 [0.712; 0.896] with the sensitivity and the specificity of 0.863 and 0.618, respectively. αSyn in AD patients does not differentiate between subjects with- and without EP. Its increased average concentration reflects probably neurodegenerative process, and is not specific for any pathophysiologic mechanisms. Further studies are necessary to explain the role of CSF αSyn as a potential biomarker.

وصف الملف: application/pdf

العلاقة: https://opus4.kobv.de/opus4-fau/frontdoor/index/index/docId/22223Test; urn:nbn:de:bvb:29-opus4-222237; https://nbn-resolving.org/urn:nbn:de:bvb:29-opus4-222237Test; https://doi.org/10.1007/s00702-021-02351-xTest; https://opus4.kobv.de/opus4-fau/files/22223/s00702-021-02351-x.pdfTest

الإتاحة: https://doi.org/10.1007/s00702-021-02351-xTest
https://opus4.kobv.de/opus4-fau/frontdoor/index/index/docId/22223Test
https://nbn-resolving.org/urn:nbn:de:bvb:29-opus4-222237Test
https://opus4.kobv.de/opus4-fau/files/22223/s00702-021-02351-x.pdfTest

المؤلفون: Kac, Przemyslaw R., González-Ortiz, Fernándo, 1990, Emeršič, Andreja, Dulewicz, Maciej, 1990, Koutarapu, Srinivas, Turton, Michael, An, Yang, Smirnov, Denis, Kulczyńska-Przybik, Agnieszka, Varma, Vijay, Ashton, Nicholas J., Montoliu-Gaya, Laia, Camporesi, Elena, Winkel, Izabela, Paradowski, Bogusław, Moghekar, Abhay, Troncoso, Juan C, Brinkmalm, Gunnar, Resnick, Susan M, Mroczko, Barbara, Kvartsberg, Hlin, 1987, Gregorič Kramberger, Milica, Hanrieder, Jörg, 1980, Čučnik, Saša, Harrison, Peter, Zetterberg, Henrik, 1973, Lewczuk, Piotr, Thambisetty, Madhav, Rot, Uroš, Galasko, Douglas, Blennow, Kaj, 1958, Karikari, Thomas

المصدر: medRxiv : the preprint server for health sciences.

مصطلحات موضوعية: Neurosciences, Neurovetenskaper

الوصف: Blood phosphorylated tau (p-tau) biomarkers, including p-tau217, show high associations with Alzheimer's disease (AD) neuropathologic change and clinical stage. Certain plasma p-tau217 assays recognize tau forms phosphorylated additionally at threonine-212, but the contribution of p-tau212 alone to AD is unknown. We developed a blood-based immunoassay that is specific to p-tau212 without cross-reactivity to p-tau217. Thereafter, we examined the diagnostic utility of plasma p-tau212. In five cohorts (n=388 participants), plasma p-tau212 showed high performances for AD diagnosis and for the detection of both amyloid and tau pathology, including at autopsy as well as in memory clinic populations. The diagnostic accuracy and fold changes of plasma p-tau212 were similar to those for p-tau217 but higher than p-tau181 and p-tau231. Immunofluorescent staining of brain tissue slices showed prominent p-tau212 reactivity in neurofibrillary tangles that co-localized with p-tau217 and p-tau202/205. These findings support plasma p-tau212 as a novel peripherally accessible biomarker of AD pathophysiology.

الوصول الحر: https://gup.ub.gu.se/publication/333144Test

المؤلفون: Sims, John R., Zimmer, Jennifer A., Evans, Cynthia D., Lu, Ming, Ardayfio, Paul, Sparks, JonDavid, Wessels, Alette M., Shcherbinin, Sergey, Wang, Hong, Monkul Nery, Emel Serap, Collins, Emily C., Solomon, Paul, Salloway, Stephen, Apostolova, Liana G., Hansson, Oskar, Ritchie, Craig, Brooks, Dawn A., Mintun, Mark, Skovronsky, Daniel M., Abreu, Rafael, Agarwal, Pinky, Aggarwal, Puja, Agronin, Marc, Allen, Alison, Altamirano, Dario, Alva, Gustavo, Andersen, James, Anderson, Allan, Anderson, Donald, Arnold, Jennifer, Asada, Takashi, Aso, Yasuhiro, Atit, Vikram, Ayala, Ricardo, Badruddoja, Michael, Badzio-jagiello, Hanna, Bajacek, Michal, Barton, David, Bear, David, Benjamin, Sabrina, Bergeron, Richard, Bhatia, Perminder, Black, Sandra, Block, Allan, Bolouri, Mohammad, Bond, Wendy, Bouthillier, Jean, Brangman, Sharon, Brew, Bruce, Brisbin, Sarah, Brisken, Toby, Brodtmann, Amy, Brody, Mark, Brosch, Jared, Brown, Celia, Brownstone, Paul, Bukowczan, Sylwia, Burns, Jeffrey, Cabrera, Alicia, Capote, Horace, Carrasco, Angel, Cevallos Yepez, Jose, Chavez, Eric, Chertkow, Howard, Chyrchel-paszkiewicz, Urszula, Ciabarra, Anthony, Clemmons, Edward, Cohen, Daniel, Cohen, Robert, Cohen, Ian, Concha, Mauricio, Costell, Brian, Crimmins, Denis, Cruz-pagan, Yvette, Cueli, Adolfo, Cupelo, Robert, Czarnecki, Maciej, Darby, David, Dautzenberg, P.l.j., De Deyn, Peter Paul, De La Gandara, Jose, Deck, Kenneth, Dibenedetto, David, Dibuono, Mark, Dinnerstein, Eric, Dirican, Ahmet, Dixit, Shanker, Dobryniewski, Jacek, Drake, Ryan, Drysdale, Peter, Duara, Ranjan, Duffy, John, Ellenbogen, Aaron, Faradji, Victor, Feinberg, Marc, Feldman, Robert, Fishman, Simon, Flitman, Stephen, Forchetti, Concetta, Fraga, Ivonne, Frank, Andrew, Frishberg, Benjamin, Fujigasaki, Fukase, Hiroyuki, Fumero, Ileana, Furihata, Kenichi, Galloway, Christopher, Gandhi, Rekha, George, Kristi, Germain, Marcel, Gitelman, Darren, Goetsch, Nicholas, Goldfarb, Danielle, Goldstein, Mark, Goldstick, Lawrence, Gonzalez Rojas, Yaneicy, Goodman, Ira, Greeley, David, Griffin, Carl, Grigsby, Eric, Grosz, Daniel, Hafner, Karl, Hart, David, Henein, Sam, Herskowitz, Brad, Higashi, Shinji, Higashi, Yasuto, Ho, Gilbert, Hodgson, Jonathan, Hohenberg, Mark, Hollenbeck, Larry, Holub, Richard, Hori, Tomokatsu, Hort, Jakub, Ilkowski, Jan, Ingram, K. Jennifer, Isaac, Mitchell, Ishikawa, Mitsunori, Janu, Lubos, Johnston, Mark, Julio, William, Justiz, William, Kaga, Tomotsugu, Kakigi, Tatsuya, Kalafer, Marvin, Kamijo, Mikiko, Kaplan, Jeffrey, Karathanos, Michael, Katayama, Sadao, Kaul, Siddharth, Keegan, Andrew, Kerwin, Diana, Khan, Uzma, Khan, Arifulla, Kimura, Noriyuki, Kirk, Gregory, Klodowska, Gabriela, Kowa, Hisatomo, Kutz, Christen, Kwentus, Joseph, Lai, Rosalyn, Lall, Ayesha, Lawrence, Mary, Lee, Elly, Leon, Ramon, Linker, Gary, Lisewski, Pawel, Liss, Jonathan, Liu, Collins, Losk, Scott, Lukaszyk, Ewelina, Lynch, Jennifer, Macfarlane, Stephen, Macsweeney, Josephine, Mannering, Nicholas, Markovic, Oto, Marks, Donald, Masdeu, Joseph, Matsui, Yutaka, Matsuishi, Kunitaka, Mcallister, Peter, Mcconnehey, Brock, Mcelveen, Alvin, Mcgill, Lora, Mecca, Adam, Mega, Michael, Mensah, Jason, Mickielewicz, Anatol, Minaeian, Artin, Mocherla, Bharat, Murphy, Cynthia, Murphy, Paul, Nagashima, Hirotaka, Nair, Anil, Nair, Malini, Nardandrea, John, Nash, Marshall, Nasreddine, Ziad, Nishida, Yoshihiko, Norton, Jeffrey, Nunez, Lazaro, Ochiai, Jun, Ohkubo, Takuya, Okamura, Yasuyuki, Okorie, Eugene, Olivera, Esteban, O'mahony, John, Omidvar, Omid, Ortiz-Cruz, Desiree, Osowa, Alexander, Papka, Michelle, Parker, Alicia, Patel, Paayal, Patel, Ashok, Patel, Meenakshi, Patry, Claude, Peckham, Elizabeth, Pfeffer, Michael, Pietras, Alison, Plopper, Michael, Porsteinsson, Anton, Poulin Robitaille, Raphael, Prins, Niels, Puente, Orlando, Ratajczak, Marcin, Rhee, Margaret, Ritter, Angela, Rodriguez, Ramon, Rodriguez Ables, Lilia, Rojas, Julio, Ross, Jeffrey, Royer, Paule, Rubin, Jay, Russell, David, Rutgers, Sterre Malou, Rutrick, Stephanie, Sadowski, Martin, Safirstein, Beth, Sagisaka, Takafumi, Scharre, Douglas, Schneider, Lon, Schreiber, Curtis, Schrift, Michael, Schulz, Paul, Schwartz, Harvey, Schwartzbard, Julie, Scott, John, Selem, Lissette, Sethi, Pramod, Sha, Sharon, Sharlin, Kenneth, Sharma, Sanjiv, Shiovitz, Thomas, Shiwach, Rajinder, Sladek, Martin, Sloan, Bart, Sorial, Ehab, Sosa, Evelio, Stedman, Mary, Steen, Susan, Stein, Lee, Stolyar, Arkadiy, Stoukides, John, Sudoh, Shinji, Sutton, James, Syed, Junaid, Szigeti, Kinga, Tachibana, Hisatsugu, Takahashi, Yuichi, Tateno, Amane, Taylor, James Dale, Taylor, Kelly, Tcheremissine, Oleg, Thebaud, Adly, Thein, Stephen, Thurman, Louise, Toenjes, Steven, Toji, Hiromasa, Toma, Misaki, Tran, Duc, Tsujimoto, Masashi, Turner, Raymond, Uchiyama, Akiyoshi, Ussorowska, Dorota, Vaishnavi, Sanjeev, Valor, Elena, Vandersluis, Joel, Vasquez, Alberto, Velez, Juan, Verghese, Cherian, Vodickova-borzova, Klaudia, Watson, David, Weidman, David, Weisman, David, White, Alexander, Willingham, Katherine, Winkel, Izabela, Winner, Paul, Winston, Jaron, Wolff, Adam, Yagi, Hideo, Yamamoto, Hideki, Yathiraj, Sanjay, Yoshiyama, Yasumasa, Zboch, Marzena

المساهمون: TRAILBLAZER-ALZ 2 Investigators

المصدر: 0098-7484 ; JAMA : the journal of the American Medical Association

مصطلحات موضوعية: Chemistry, Biology, Human medicine

الوصف: Importance There are limited efficacious treatments for Alzheimer disease. Objective To assess efficacy and adverse events of donanemab, an antibody designed to clear brain amyloid plaque. Design, Setting, and Participants Multicenter (277 medical research centers/hospitals in 8 countries), randomized, double-blind, placebo-controlled, 18-month phase 3 trial that enrolled 1736 participants with early symptomatic Alzheimer disease (mild cognitive impairment/mild dementia) with amyloid and low/medium or high tau pathology based on positron emission tomography imaging from June 2020 to November 2021 (last patient visit for primary outcome in April 2023). Interventions Participants were randomized in a 1:1 ratio to receive donanemab (n = 860) or placebo (n = 876) intravenously every 4 weeks for 72 weeks. Participants in the donanemab group were switched to receive placebo in a blinded manner if dose completion criteria were met. Main Outcomes and Measures The primary outcome was change in integrated Alzheimer Disease Rating Scale (iADRS) score from baseline to 76 weeks (range, 0-144; lower scores indicate greater impairment). There were 24 gated outcomes (primary, secondary, and exploratory), including the secondary outcome of change in the sum of boxes of the Clinical Dementia Rating Scale (CDR-SB) score (range, 0-18; higher scores indicate greater impairment). Statistical testing allocated α of .04 to testing low/medium tau population outcomes, with the remainder (.01) for combined population outcomes. Results Among 1736 randomized participants (mean age, 73.0 years; 996 [57.4%] women; 1182 [68.1%] with low/medium tau pathology and 552 [31.8%] with high tau pathology), 1320 (76%) completed the trial. Of the 24 gated outcomes, 23 were statistically significant. The least-squares mean (LSM) change in iADRS score at 76 weeks was −6.02 (95% CI, −7.01 to −5.03) in the donanemab group and −9.27 (95% CI, −10.23 to −8.31) in the placebo group (difference, 3.25 [95% CI, 1.88-4.62]; P < .001) in the low/medium ...

الإتاحة: https://doi.org/10.1001/JAMA.2023.13239Test
https://hdl.handle.net/10067/1979740151162165141Test

المؤلفون: Winkel Izabela, Sobieszczańska Malgorzata, Kołodziej Małgorzata, Lindner Karolina, Rohan Anna, Fugiel Jarosław

المصدر: Experimental aging research. 48(4)

مصطلحات موضوعية: Functional training, medicine.medical_specialty, Aging, Cognition, medicine.disease, Conceptual thinking, Hand movements, Physical medicine and rehabilitation, Arts and Humanities (miscellaneous), Walk test, medicine, Dementia, Humans, Geriatrics and Gerontology, Cognitive impairment, Psychology, Cognition Disorders, Exercise, General Psychology, Fine motor

الوصف: OBJECTIVES to assess and compare the gross and fine motor skills in people with identified cognitive impairment and in people from the control group. METHOD The research was conducted at the Center of Dementia-Related Diseases, involved participants with (n = 39) and without (n = 29) cognitive disorders. Fast, precise hand movements were measured via Vienna System Test. The up-and-go, chair-stand, 6-minute walk tests were used to assess functional fitness. The results for participants with and without cognitive disorders were compared. RESULTS People from both groups do not differ significantly in terms of the level of condition-based functional fitness. Participants with cognitive disorders achieve worse results in hand coordination tests which are more complex and require both speed and accuracy of hand movements. DISCUSSION The deterioration of precise hand movements with the correct functional efficiency may indicate degenerative changes in brain areas associated with complex thought processes, conceptual thinking, and may lead to dementia.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c62a47ca6e759b22b25ff0cdbf727e6eTest
https://pubmed.ncbi.nlm.nih.gov/34605367Test

المؤلفون: Jeżowska, Klaudia, Pokryszko-Dragan, Anna, Budrewicz, Sławomir, Zimny, Anna, Winkel, Izabela, Żelwetro, Agnieszka, Tyfel, Paweł, Jurczyk, Piotr, Podemski, Ryszard

المصدر: Polski Przegląd Neurologiczny; Vol 12, No 4 (2016); 211-216

مصطلحات موضوعية: zanik korowy-tylny, zespół korowo-podstawny, zespoły nakładania

الوصف: Zespół nakładania chorób neurozwyrodnieniowych to współwystępowanie objawów klinicznych lub zmian histopatologicznych typowych dla różnych schorzeń z tej grupy u jednego chorego. Złożony obraz kliniczny zespołów nakładania może stwarzać trudności diagnostyczne i lecznicze. Autorzy przedstawiają przypadek 64-letniej chorej z rozpoznaniem zaniku korowego tylnego (wariant wzrokowy choroby Alzheimera), do którego po kilku latach dołączyły się objawy zespołu korowo-podstawnego.

وصف الملف: application/pdf

العلاقة: https://journals.viamedica.pl/polski_przeglad_neurologiczny/article/view/50691Test

الإتاحة: https://journals.viamedica.pl/polski_przeglad_neurologiczny/article/view/50691Test

المؤلفون: Winkel, Izabela, Lewczuk, Piotr, Zboch, Marzena, Żelwetro, Agnieszka

المصدر: Polski Przegląd Neurologiczny; Vol 10, No 2 (2014); 83-87

مصطلحات موضوعية: otępienie, choroba Alzheimera, PCA, zaburzenia wzrokowo-przestrzenne

الوصف: Choroba Alzheimera (AD, Alzheimer’s disease) jest najbardziej powszechnym schorzeniem neurozwyrodnieniowym mózgu. Jej osiowym objawem są postępujące zaburzenia pamięci. Należy brać pod uwagę także inne warianty tej choroby, takie jak: wariant wzrokowy (PCA, posterior cortical atrophy), czołowy, językowy i wariant z ciałami Lewy’ego, różniące się między sobą obrazem klinicznym i w których nie dominują deficyty pamięci. W artykule przedstawiono wzrokowy wariant AD, który jest zespołem objawów klinicznych z dominującymi dysfunkcjami wzrokowo-przestrzennymi, ze stosunkowo dobrze zachowanymi procesami mnestycznymi. Zaprezentowano także schemat diagnostyczny, cechy kliniczne i przebieg atypowej postaci AD. Podłożem PCA w większości przypadków jest patologia alzheimerowska. Dla ustalenia rozpoznania i wyboru odpowiedniej strategii terapeutycznej kluczowe znaczenie mają ocena neuropsychologiczna oraz badanie biomarkerów procesu neurozwyrodnieniowego w płynie mózgowo-rdzeniowym.

وصف الملف: application/pdf

العلاقة: https://journals.viamedica.pl/polski_przeglad_neurologiczny/article/view/39229Test

الإتاحة: https://journals.viamedica.pl/polski_przeglad_neurologiczny/article/view/39229Test