Abstract
Missense mutations in presenilin 1 (PSNL1) are known to cause familial Alzheimer's disease which is a subtype of Alzheimer's disease (AD). Our investigation, using an in situ hybridization technique, indicated that the localization of PSNL1 mRNA is similar in sporadic AD affected and normal human brains. Furthermore, the amounts of PSNL1 mRNA in neurofibrillary tangle (NFT)-bearing neurons and those without NFTs did not differ, and the clinical severity of AD was not related to PSNL1 mRNA expression level.
MeSH terms
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Aged
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Aged, 80 and over
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Alzheimer Disease / genetics*
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Alzheimer Disease / pathology
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Autoradiography
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DNA, Antisense
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Family Health
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Hippocampus / metabolism*
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Hippocampus / pathology
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Humans
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In Situ Hybridization
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Membrane Proteins / genetics*
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Middle Aged
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Neurofibrillary Tangles / genetics
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Neurofibrillary Tangles / metabolism
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Neurofilament Proteins / genetics
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Polymerase Chain Reaction
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Presenilin-1
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RNA, Messenger / metabolism
Substances
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DNA, Antisense
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Membrane Proteins
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Neurofilament Proteins
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PSEN1 protein, human
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Presenilin-1
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RNA, Messenger