Neurol Ther (2018) 7:1–3 https://doi.org/10.1007/s40120-018-0100-5 EDITORIAL Editorial Regarding: Practical Treatment of Lewy Body Disease in the Clinic: Patient and Physician Perspectives Thomas Mu ¨ ller Received: February 27, 2018 / Published online: April 27, 2018 The Author(s) 2018 Keywords: Alzheimer’s disease; Lewy body focuses on the amelioration of the quality of life dementia; Parkinson’s disease dementia for patients and their caregivers, quite often only trying to delay life in a nursing home. Standardised guidelines based on so-called evi- Alzheimer’s disease, Lewy body dementia, dence-based analyses of trials are of limited Parkinson’s disease dementia, vascular demen- value. Off-label use of drugs is common. tia, and vascular Parkinsonism are frequently One should not forget that the employed occuring syndromes of chronic brain neurode- assessment instruments, as in this case, are only generation. They cause an enormous burden for sensitive and valuable to a certain extent. In this healthcare. All these terms reﬂect disease enti- respect, the MiniMentalStateExamination rep- ties; in other words, they are not speciﬁc, and resents just a screening tool, which is overesti- their features and progression overlap. Thus, mated and therefore under debate [1, 2]. their drug treatment needs an individually Performance of these tests suffers from addi- adapted not a standardised regimen. tional factors, such as motivation, education Therefore, in academia, speciﬁc well-deﬁned and personality features. diagnosis criteria only partially and artiﬁcially Moreover, the onset and features of these syn- reﬂect the whole spectrum of signs observed in dromes of cholinergic and dopaminergic deﬁ- the clinic. Drug treatment of these patients ciency are heterogeneous; pure forms rarely exist. The most common form is a mixture of all the Editorial regarding the article by Londos, E., Neurol Ther discussed syndromes, often based on a predomi- (2017) https://doi.org/10.1007/s40120-017-0090-8, Let- nant vascular origin. Mostly, patients also suffer ter to the Editor by Brzezicki, M., Neurol Ther (2018) from additional disorders, which may aggravate or https://doi.org/10.1007/s40120-018-0098-8 and Author’s Response: Londos, E., (2018) https://doi.org/10. even induce cognitive dysfunction, or falsely imi- 1007/s40120-018-0099-7. tate cognitive deterioration, i.e. in the case of the additional onset of depression or apathy. Enhanced digital content To view enhanced digital To date, it is far from clear whether Lewy body content for this article go to https://doi.org/10.6084/ m9.ﬁgshare.6099452. accumulation or ß-amyloid or tau protein enrichment play any active role in the ongoing T. Mu ¨ ller (&) chronic disease process itself in the affected neu- Department of Neurology, St. Joseph Hospital rons. They may also just represent well-wrapped Berlin-Weissensee, Gartenstr. 1, 13088 Berlin, protein garbage as a consequence of disease-af- Germany fected neurons . Chronic neurodegeneration is e-mail: firstname.lastname@example.org; email@example.com 2 Neurol Ther (2018) 7:1–3 a result of different metabolic cascades. They Authorship. All named authors meet the ﬁnally end up in cell death-inducing events and, International Committee of Medical Journal accordingly, individually different clinical signs. Editors (ICMJE) criteria for authorship for this Nowadays, research on the causes of neurode- article, take responsibility for the integrity of generation still focus on hypotheses based on the work as a whole, and have given their neuropathological ﬁndings. Many of them sup- approval for this version to be published. port the concepts of protein misfolding. Gener- Disclosures. Thomas Mu ¨ ller has nothing to ally, when protein misfolding occurs, the ﬁrst line disclose. of defense involves refolding, a process mediated by chaperone proteins. If the process of refolding Compliance with Ethics Guidelines. This fails, these misfolded proteins will either be article is based on previously conducted studies degraded or will accumulate. When the refolding/ and does not contain any studies with human degradation machinery is unable to process mis- participants or animals performed by any of the folded proteins, a stress response is activated that authors. involves upregulation of refolding and degrada- tion processes . If the misfolded protein stress is Open Access. This article is distributed too severe, cell death programs may be activated. under the terms of the Creative Commons Accordingly, potential strategies are the reduction Attribution-NonCommercial 4.0 International of protein misfolding, the repair of misfolded License (http://creativecommons.org/licenses/ proteins and the facilitation of the degradation of by-nc/4.0/), which permits any noncommer- proteins which are thus damaged without any cial use, distribution, and reproduction in any chance for repair. However, there is a certain medium, provided you give appropriate credit capacity of the human brain to compensate these to the original author(s) and the source, provide initial events for a considerable interval before the a link to the Creative Commons license, and clinical onset of initial mild and unspeciﬁc indicate if changes were made. symptoms of neurodegenerative disease. Thus, the velocity of disease progression also differs in an individually different manner. Preclinical and experimental researchers still primarily focus on REFERENCES the acetylcholine—respectively, dopamine deﬁcit and related behavioural changes. They do not 1. Larner AJ. Correlation or limits of agreement? apply- consider the individually different decline of ing the Bland–Altman approach to the comparison of other neurotransmitter systems, like 5-HT, nore- cognitive screening instruments. Dement Geriatr pinephrine, etc. These are the main reasons why Cogn Disord. 2016;42(5–6):247–54. therapeutic interventions on tau- and ß-amyloid 2. Seigerschmidt E, Mosch E, Siemen M, Forstl H, Bickel metabolism has failed in clinical trials. H. The clock drawing test and questionable dementia: In this respect, the discussion here [5–7]isa reliability and validity. Int J Geriatr Psychiatry. typical example of the missing reality of aca- 2002;17(11):1048–54. demic research and so-called evidence-based 3. Sian-Hulsmann J, Monoranu C, Strobel S, Riederer P. medicine for the daily maintenance of these Lewy bodies: a spectator or salient killer? CNS Neurol patients. Disord Drug Targets. 2015;14(7):947–55. 4. Kumar P, Jha NK, Jha SK, Ramani K, Ambasta RK. Tau phosphorylation, molecular chaperones, and ubiqui- ACKNOWLEDGEMENTS tin E3 ligase: clinical relevance in Alzheimer’s disease. J Alzheimers Dis. 2015;43(2):341–61. 5. Londos E. Practical treatment of lewy body disease in the Funding. No funding or sponsorship was clinic: patient and physician perspectives. Neurol Ther. received for this study or publication of this article. 2017. https://doi.org/10.1007/s40120-017-0090-8. Neurol Ther (2018) 7:1–3 3 6. Brzezicki MA, Kobetic ´ MD. Letter to the editor 7. Londos E. Author’s response to the letter to the editor regarding: practical treatment of Lewy body disease regarding: practical treatment of Lewy body disease in in the clinic: patient and physician perspectives. the clinic: patient and physician perspectives. Neurol Neurol Ther. 2018. https://doi.org/10.1007/s40120- Ther. 2018. https://doi.org/10.1007/s40120-018-0099-7 018-0098-8.
Neurology and Therapy – Springer Journals
Published: Apr 27, 2018
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