Parkinsonism in genetic and sporadic Alzheimer's disease

被引:2
|
作者
Levin, Johannes [1 ]
机构
[1] Ludwig Maximilians Univ Munchen, Deutsch Zentrum Neurodegenerat Erkrankungen DZNE, Munich Cluster Syst Neurol SyNergy, Dept Neurol, Munich, Germany
来源
PARKINSONISM BEYOND PARKINSON'S DISEASE | 2019年 / 149卷
关键词
ASSOCIATION WORKGROUPS; DIAGNOSTIC GUIDELINES; NATIONAL INSTITUTE; LEWY BODIES; MOTOR SIGNS; DEMENTIA; RECOMMENDATIONS; CRITERIA;
D O I
10.1016/bs.irn.2019.10.005
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Alzheimer disease (AD) is a neurodegenerative disease characterized by deposition of pathologically aggregated amyloid-beta in the extracellular space and pathologically aggregated tau protein in the intracellular space. Mainly affected brain areas are the temporal and the parietal lobe, which cause the classical AD phenotype consisting of increasing forgetfulness and difficulties to orientate. However, AD pathology is not restricted to these brain areas and spreads through the brain as the disease progresses, which can lead to a number of additional symptoms and to atypical presentations. Motor symptoms in AD are the topic of this chapter. Even though motor symptoms are usually not severe and seldomly treated, motor symptoms are quite frequent and can be observed in the majority of AD cases. Motor symptoms are especially frequent in cases with early onset and long disease duration, for example in Apolipoprotein E e4 carriers and in familial early onset AD. In severe cases treatment with pharmacological approaches might be considered. However, treatment strategies largely rely on expert opinions. Due to potential positive impact on prognosis non-pharmacological treatment and exercise might be considered in less advanced cases.
引用
收藏
页码:237 / 247
页数:11
相关论文
共 50 条
  • [1] Mitochondrial dysfunction in sporadic and genetic Alzheimer's disease
    Hauptmann, Susanne
    Keil, Uta
    Scherping, Isabel
    Bonert, Astrid
    Eckert, Anne
    Mueller, Walter E.
    EXPERIMENTAL GERONTOLOGY, 2006, 41 (07) : 668 - 673
  • [2] Biological and genetic markers of sporadic Alzheimer's disease
    Engelborghs, S
    De Deyn, PP
    ACTA MEDICA OKAYAMA, 2001, 55 (02) : 55 - 63
  • [3] Genetic Variants and Related Biomarkers in Sporadic Alzheimer’s Disease
    Rita Guerreiro
    Jose Bras
    Jamie Toombs
    Amanda Heslegrave
    John Hardy
    Henrik Zetterberg
    Current Genetic Medicine Reports, 2015, 3 (1) : 19 - 25
  • [4] Increased apoptotic cell death in sporadic and genetic Alzheimer's disease
    Eckert, A
    Marques, CA
    Keil, U
    Schüssel, K
    Müller, WE
    APOPTOSIS: FROM SIGNALING PATHWAYS TO THERAPEUTIC TOOLS, 2003, 1010 : 604 - 609
  • [5] Neuropathology of Parkinsonism in Alzheimer's Disease
    Kovari, Eniko
    Bouras, Constantin
    Herrmann, Francois R.
    Burkhard, Pierre R.
    Horvath, Judit
    Xekardaki, Aikaterini
    GENEDIS 2014: NEURODEGENERATION, 2015, 822 : 149 - 149
  • [6] MITOPHAGY AND SPORADIC ALZHEIMER'S DISEASE
    Vrajova, Monika
    AGEING 2018, 2018, : 178 - 183
  • [7] Epistasis in sporadic Alzheimer's disease
    Combarros, Onofre
    Cortina-Borja, Mario
    Smith, A. David
    Lehmann, Donald J.
    NEUROBIOLOGY OF AGING, 2009, 30 (09) : 1333 - 1349
  • [8] Modelling sporadic Alzheimer's disease
    Salkovic, M.
    Gruennblatt, E.
    Osmanovic, J.
    Hoyer, S.
    Riederer, P.
    JOURNAL OF NEURAL TRANSMISSION, 2007, 114 (07) : CIX - CIX
  • [9] Neurosteroids and sporadic Alzheimer's disease
    Barry, Guy
    Ross, Ian L.
    CURRENT ALZHEIMER RESEARCH, 2008, 5 (04) : 367 - 374
  • [10] An essential variable for the definition of genetic risk factors for sporadic Alzheimer's disease
    Beyer, K
    Lao, JI
    Latorre, P
    Ariza, A
    REVERSAL OF AGING: RESETTING THE PINEAL CLOCK, 2005, 1057 : 260 - 278