Alzheimer's disease

被引:45
作者
Turner, R. Scott
机构
[1] VA Ann Arbor Healtcare Syst, GRECC 11G, Neurol Serv, Ann Arbor, MI 48105 USA
[2] VA Geriatr Res Educ & Clin Ctr, Ann Arbor, MI USA
[3] Univ Michigan, Dept Neurol, Ann Arbor, MI 48109 USA
关键词
A beta; Alzheimer's disease; amyloid plaque; dementia; mild cognitive impairment; presenilin; tau; neurofibrillary tangle; acetylcholinesterase inhibitor; memantine;
D O I
10.1055/s-2006-951622
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Alzheimer's disease (AD) is the most commonly diagnosed etiology of dementia and may be caused by the progressive accumulation and deposition of neurotoxic A beta/amyloid plaques and aggregates in brain with aging-the amylold hypothesis of AD. However, A beta/amyloid deposition is likely necessary but not sufficient to cause AD, and other putative downstream pathologies, including the aggregation of phospho-tau in neurofibrillary tangles, synaptic and neuronal loss, and glial and inflammatory responses, are likely equally important to AD pathogenesis. The majority of AD is sporadic (> 95%) but the discovery of rare early onset familial forms of AD has been pivotal to our understanding of its pathogenesis and in developing novel therapeutic strategies. Currently available drugs for patients with AD provide modest, temporary, and palliative benefits, but they consistently demonstrate safety and efficacy on cognitive, functional, behavioral, and global outcome measures. Novel potential disease-modifying therapies now in preclinical research or clinical trials may be more effective in preventing or arresting the progressive dementia of AD and will provide a test of the amyloid hypothesis.
引用
收藏
页码:499 / 506
页数:8
相关论文
共 46 条
[1]  
Alzheimer A., 1907, ALLG Z PSYCHIAT, V64, P146, DOI DOI 10.1002/CA.980080612
[2]  
Alzheimers Assoc, 1998, NEUROBIOL AGING, V19, P109
[3]  
[Anonymous], 1997, Neurobiol Aging, V18, pS1
[4]  
BERTRAM L, 2006, ALZGENE DATABASE
[5]   NEUROPATHOLOGICAL STAGING OF ALZHEIMER-RELATED CHANGES [J].
BRAAK, H ;
BRAAK, E .
ACTA NEUROPATHOLOGICA, 1991, 82 (04) :239-259
[6]  
Cruts M., 2006, Alzheimer disease frontotemporal dementia mutation database
[7]  
DAVIES P, 1976, LANCET, V2, P1403
[8]   A novel presenilin 1 mutation associated with Pick's disease but not β-amyloid plaques [J].
Dermaut, B ;
Kumar-Singh, S ;
Engelborghs, S ;
Theuns, J ;
Rademakers, R ;
Sacrens, J ;
Pickut, BA ;
Peeters, K ;
van den Broeck, M ;
Vennekens, K ;
Claes, S ;
Cruts, M ;
Cras, P ;
Martin, JJ ;
Van Broeckhoven, C ;
De Deyn, PP .
ANNALS OF NEUROLOGY, 2004, 55 (05) :617-626
[9]   Secretases as targets for the treatment of Alzheimer's disease: the prospects [J].
Dewachter, I ;
Van Leuven, F .
LANCET NEUROLOGY, 2002, 1 (07) :409-416
[10]   Practice parameter: Management of dementia (an evidence-based review) - Report of the Quality Standards Subcommittee of the American Academy of Neurology [J].
Doody, RS ;
Stevens, JC ;
Beck, C ;
Dubinsky, RM ;
Kaye, JA ;
Gwyther, L ;
Mohs, RC ;
Thal, LJ ;
Whitehouse, PJ ;
DeKosky, ST ;
Cummings, JL .
NEUROLOGY, 2001, 56 (09) :1154-1166