Abnormal Sp1 transcription factor expression in Alzheimer disease and tauopathies
Abstract
Sp1 transcription factor expression was examined by immunohistochemistry, immunofluorescence and confocal microscopy in Alzheimer disease (AD), Pick disease (PiD), progressive supranuclear palsy (PSP), Parkinson disease (PD) and Dementia with Lewy bodies (DLB). Sp1 partly co-localizes with hyper-phosphorylated tau deposits in neurofibrillary tangles, dystrophic neurites of senile plaques and neuropil threads in AD, and in neurons, astrocytes and oligodendrocytes bearing hyper-phosphorylated tau in PiD and PSP. Sp1 is not found in alpha-synuclein inclusions in PD and DLB. These modifications are not associated with changes in the total expression levels of Sp1, as revealed with gel electrophoresis and Western blotting of brain homogenates. Furthermore, no co-immunoprecipitation of Sp1 and phospho-tau was observed in AD and PiD cases. Since Sp1 binding sites are present in the promoters of several genes involved in amyloid and tau, and Sp1 is regulated by oxidative stress, the present findings suggest that Sp1 deposition in hyper-phosphorylated tau deposits may have functional consequences in the pathology of AD and other tauopathies.
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SP1, a transcription factor that regulates the expression of several amyloid and tau-related genes, has been found to be abnormally expressed in the frontal cortex and hippocampus of patients with AD.
“It is noteworthy that SP1, a transcription factor that regulates the expression of several amyloid and tau-related genes,47 has been found to be abnormally expressed in the frontal cortex and hippocampus of patients with AD.48”
From APOE*E2 allele delays age of onset in PSEN1 E280A Alzheimer’s disease (2016) · cites this paper as [48]
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- Authors
- Santpere, G., Nieto, M., Puig, B., & Ferrer, I.
- Affiliations
- Bellvitge University Hospital (ES)
- Corresponding author
- Ferrer, I.
- Venue
- Neuroscience Letters
- Publisher
- Elsevier BV
- Published
- 2006-04
- Volume
- 397
- Issue
- 1-2
- Pages
- 30-34
- ISSN
- 0304-3940 (ISSN-L)
- OpenAlex
- W2038838498
- Cited by
- 70
- References
- 26
- Citations by year
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- FWCI
- 1.20
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience Letters (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Sp1, Alzheimer's disease, tauopathy, Pick's disease, progressive supranuclear palsy, Parkinson's disease, dementia with Lewy bodies, hyperphosphorylated tau, neurofibrillary tangles, amyloid plaques, neuropil threads, alpha-synuclein inclusions, oxidative stress, gene expression regulation
- MeSH terms
- Alzheimer Disease, Astrocytes, Humans, Immunohistochemistry, Neurons, Postmortem Changes, Blotting, Western, Gene Expression, Case-Control Studies, Sp1 Transcription Factor, Neurofibrillary Tangles, tau Proteins, Pick Disease of the Brain, Tauopathies, Immunoprecipitation
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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