Biological mechanisms, cerebrovascular alterations and pharmacological targets in the pathology of dementia

被引:2
作者
Albensi, BC [1 ]
机构
[1] Cleveland Clin Fdn, Cerebrovasc Res Ctr, Dept Neurol Surg, Cleveland, OH 44195 USA
关键词
D O I
10.1358/dnp.2002.15.6.701653
中图分类号
R9 [药学];
学科分类号
1007 [药学];
摘要
In response to stimulation, information is stored in the brain when synapses are simultaneously active. Interestingly, a physiological continuum may exist between processes of memory formation and brain injury, as many of the molecular mechanisms involved in memory encoding are the same as those activated during excitotoxic events in neurons. However, how brain injury leads to long lasting impairments in memory and/or dementia is still open for debate. Furthermore, evidence now suggests that cerebrovascular alterations and the pathology seen in dementia from Alzheimer's disease are mechanistically linked. Investigations have generated a wealth of information on mechanisms that become disturbed in dementia. However, there is still no cure for dementia of the Alzheimer's type. Undaunted by failures or drugs that have only modest effects, hundreds of drug discovery programs across the world continue to look for promising and more effective treatments for the disease. (C) 2002 Prous Science. All rights reserved.
引用
收藏
页码:333 / 337
页数:5
相关论文
共 9 条
[1]
LONG-LASTING POTENTIATION OF SYNAPTIC TRANSMISSION IN DENTATE AREA OF ANESTHETIZED RABBIT FOLLOWING STIMULATION OF PERFORANT PATH [J].
BLISS, TVP ;
LOMO, T .
JOURNAL OF PHYSIOLOGY-LONDON, 1973, 232 (02) :331-356
[2]
A SYNAPTIC MODEL OF MEMORY - LONG-TERM POTENTIATION IN THE HIPPOCAMPUS [J].
BLISS, TVP ;
COLLINGRIDGE, GL .
NATURE, 1993, 361 (6407) :31-39
[3]
Apolipoprotein E-ε4 genotype predicts a poor outcome in survivors of traumatic brain injury [J].
Friedman, G ;
Froom, P ;
Sazbon, L ;
Grinblatt, I ;
Shochina, M ;
Tsenter, J ;
Babaey, S ;
Ben Yehuda, A ;
Groswasser, Z .
NEUROLOGY, 1999, 52 (02) :244-248
[4]
The role of apolipoprotein E in Alzheimer's disease, acute brain injury and cerebrovascular disease: evidence of common mechanisms and utility of animal models [J].
Horsburgh, K ;
McCarron, MO ;
White, F ;
Nicoll, JAR .
NEUROBIOLOGY OF AGING, 2000, 21 (02) :245-255
[5]
The blood-brain barrier and cerebrovascular pathology in Alzheimer's disease [J].
Kalaria, RN .
OXIDATIVE/ENERGY METABOLISM IN NEURODEGENERATIVE DISORDERS, 1999, 893 :113-125
[6]
Cellular actions of beta-amyloid precursor protein and its soluble and fibrillogenic derivatives [J].
Mattson, MP .
PHYSIOLOGICAL REVIEWS, 1997, 77 (04) :1081-1132
[7]
McEachern JC, 1999, J NEUROSCI RES, V58, P42, DOI 10.1002/(SICI)1097-4547(19991001)58:1<42::AID-JNR6>3.0.CO
[8]
2-L
[9]
Mesulam MM, 2000, ANN NY ACAD SCI, V924, P42