Jin K, Peel AL, Mao XO, Xie L, Cottrell BA, Henshall DC, Greenberg DA.
Increased hippocampal neurogenesis in Alzheimer's disease.
Proc Natl Acad Sci U S A. 2004 Jan 6;101(1):343-7.
PubMed.
For stem cell researchers, this is an encouraging report which indicates neurogenesis in the Alzheimer's disease (AD) patient's brain. If this finding is true, just increasing the stem cell population in the patient’s brain might help to regenerate dying neurons in AD. Since we have a small-molecule compound that increases endogenous stem cell population about sixfold in 27-month-aged rats by peripheral injection, we may be able to develop an application for this drug in AD treatment.
However, as the author pointed out, APP- or PS-mutant transgenic mice show impaired rather than increased neurogenesis. Such a conflict may come from the different patient populations, namely, sporadic and familial AD, meaning if they analyze familial AD they might find different results. Furthermore, their best clear finding is an increased level of PSA-NCAM in severe AD cases, and PSA-NCAM is not necessarily a marker for neuronal progenitors because it is also expressed in reactive astrocytes (Nomura et al., 2000). Thus, we may be able to say that AD brain is still trying to regenerate its neurons, but we need further investigation to confirm if spontaneous neurogenesis really occurs in AD.
References:
Nomura T, Yabe T, Rosenthal ES, Krzan M, Schwartz JP.
PSA-NCAM distinguishes reactive astrocytes in 6-OHDA-lesioned substantia nigra from those in the striatal terminal fields.
J Neurosci Res. 2000 Sep 15;61(6):588-96.
PubMed.
Comments
University of Central Florida
For stem cell researchers, this is an encouraging report which indicates neurogenesis in the Alzheimer's disease (AD) patient's brain. If this finding is true, just increasing the stem cell population in the patient’s brain might help to regenerate dying neurons in AD. Since we have a small-molecule compound that increases endogenous stem cell population about sixfold in 27-month-aged rats by peripheral injection, we may be able to develop an application for this drug in AD treatment.
However, as the author pointed out, APP- or PS-mutant transgenic mice show impaired rather than increased neurogenesis. Such a conflict may come from the different patient populations, namely, sporadic and familial AD, meaning if they analyze familial AD they might find different results. Furthermore, their best clear finding is an increased level of PSA-NCAM in severe AD cases, and PSA-NCAM is not necessarily a marker for neuronal progenitors because it is also expressed in reactive astrocytes (Nomura et al., 2000). Thus, we may be able to say that AD brain is still trying to regenerate its neurons, but we need further investigation to confirm if spontaneous neurogenesis really occurs in AD.
References:
Nomura T, Yabe T, Rosenthal ES, Krzan M, Schwartz JP. PSA-NCAM distinguishes reactive astrocytes in 6-OHDA-lesioned substantia nigra from those in the striatal terminal fields. J Neurosci Res. 2000 Sep 15;61(6):588-96. PubMed.
View all comments by Kiminobu SugayaMake a Comment
To make a comment you must login or register.