β-Amyloid precursor protein of Alzheimer's disease in cultured bovine oligodendrocytes

1992 ◽  
Vol 32 (1) ◽  
pp. 34-42 ◽  
Author(s):  
M. Mizuguchi ◽  
K. Ikeda ◽  
Seung U. Kim
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Precursor Protein ◽  
Precursor Protein ◽  
Β Amyloid

scholarly journals Neuronal aging potentiates beta-amyloid generation via amyloid precursor protein endocytosis

2019 ◽  
Author(s):  
Tatiana Burrinha ◽  
Ricardo Gomes ◽  
Ana Paula Terrasso ◽  
Cláudia Guimas Almeida
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Precursor Protein ◽  
Precursor Protein ◽  
App Processing ◽  
Early Endosomes ◽  
Primary Mouse ◽  
Β Amyloid ◽  
Aβ Production

AbstractAging increases the risk of Alzheimer’s disease (AD). During normal aging synapses decline and β-Amyloid (Aβ) accumulates. An Aβ defective clearance with aging is postulated as responsible for Aβ accumulation, although a role for increased Aβ production with aging can also lead to Aβ accumulation. To test this hypothesis, we established a long-term culture of primary mouse neurons that mimics neuronal aging (lysosomal lipofuscin accumulation and synapse decline). Intracellular endogenous Aβ42 accumulated in aged neurites due to increased amyloid-precursor protein (APP) processing. We show that APP processing is up-regulated by a specific age-dependent increase in APP endocytosis. Endocytosed APP accumulated in early endosomes that, in turn were found augmented in aged neurites. APP processing and early endosomes up-regulation was recapitulated in vivo. Finally, we found that inhibition of Aβ production reduced the decline in synapses in aged neurons. We propose that potentiation of APP endocytosis by neuronal aging increases Aβ production, which contributes to aging-dependent decline in synapses.SummaryHow aging increases the risk of Alzheimer’s disease is not clear. We show that normal neuronal aging increases the intracellular production of β-amyloid, due to an upregulation of the amyloid precursor protein endocytosis. Importantly, increased Aβ production contributes to the aging-dependent synapse loss.

scholarly journals Comparison of Neurodegenerative Pathology in Transgenic Mice Overexpressing V717F β-Amyloid Precursor Protein and Alzheimer’s Disease

1996 ◽  
Vol 16 (18) ◽  
pp. 5795-5811 ◽  
Author(s):  
Eliezer Masliah ◽  
Abbyann Sisk ◽  
Margaret Mallory ◽  
Lennart Mucke ◽  
Dale Schenk ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Amyloid Precursor Protein ◽  
Precursor Protein ◽  
Neurodegenerative Pathology ◽  
Β Amyloid

Formation of stable complexes between two Alzheimer's disease gene products: Presenilin-2 and β-amyloid precursor protein

1997 ◽  
Vol 3 (3) ◽  
pp. 328-332 ◽  
Author(s):  
A. Weidemann ◽  
K. Paliga ◽  
U. Dürrwang ◽  
C. Czech ◽  
G. Evin ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Precursor Protein ◽  
Disease Gene ◽  
Precursor Protein ◽  
Gene Products ◽  
Presenilin 2 ◽  
Β Amyloid

Early-onset Alzheimer's disease caused by mutations at codon 717 of the β-amyloid precursor protein gene

Nature ◽  
1991 ◽  
Vol 353 (6347) ◽  
pp. 844-846 ◽  
Author(s):  
Marie-Christine Chartier-Harlin ◽  
Fiona Crawford ◽  
Henry Houlden ◽  
Andrew Warren ◽  
David Hughes ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Precursor Protein ◽  
Early Onset ◽  
Protein Gene ◽  
Precursor Protein ◽  
Amyloid Precursor Protein Gene ◽  
Early Onset Alzheimer’S Disease ◽  
Β Amyloid
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