TY - JOUR
T1 - Distinct destructive signal pathways of neuronal death in Alzheimer's disease
AU - Shen, Yong
AU - He, Ping
AU - Zhong, Zhenyu
AU - McAllister, Carrie
AU - Lindholm, Kristina
N1 - Funding Information:
We thank Ms. Gabrielle Strobel and Ms. June Kinoshita from Alzheimer Forum for their crucial assistance during the manuscript preparation. For related discussions, please see http://www.alzforum.org/res/for/journal/vincent/default.asp and http://www.alzforum.org/res/for/journal/hanawalt/default.asp . The authors are supported by Alzheimer's Association, American Health Assistance Foundation and National Institute of Aging.
PY - 2006/12
Y1 - 2006/12
N2 - Abundant neuron loss is a major feature of Alzheimer's disease (AD). Hypotheses for this loss include abnormal amyloid precursor protein processing (i.e. excess Aβ production, protein aggregation or misfolding), oxidative stress, excitotoxicity and inflammation. Neuron loss is a major cause of dementia in AD; however, it seems that there is no definitive pathway that causes cell death in the AD brain. Here, we examine the hypotheses for neuron loss in AD and pose the argument that the means by which neurons degenerate is irrelevant for cognitive decline. The best treatment for cognitive decline is to prevent the toxicity that first sets the neuron on its path to destruction, which is the production of Aβ peptide.
AB - Abundant neuron loss is a major feature of Alzheimer's disease (AD). Hypotheses for this loss include abnormal amyloid precursor protein processing (i.e. excess Aβ production, protein aggregation or misfolding), oxidative stress, excitotoxicity and inflammation. Neuron loss is a major cause of dementia in AD; however, it seems that there is no definitive pathway that causes cell death in the AD brain. Here, we examine the hypotheses for neuron loss in AD and pose the argument that the means by which neurons degenerate is irrelevant for cognitive decline. The best treatment for cognitive decline is to prevent the toxicity that first sets the neuron on its path to destruction, which is the production of Aβ peptide.
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U2 - 10.1016/j.molmed.2006.10.002
DO - 10.1016/j.molmed.2006.10.002
M3 - Article
C2 - 17055782
AN - SCOPUS:33751172145
SN - 1471-4914
VL - 12
SP - 574
EP - 579
JO - Trends in Molecular Medicine
JF - Trends in Molecular Medicine
IS - 12
ER -