The unfolded protein response is activated in disease-affected brain regions in progressive supranuclear palsy and Alzheimer’s disease
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Background: Progressive supranuclear palsy (PSP) is a neurodegenerative disorder pathologically characterized by intracellular tangles of hyperphosphorylated tau protein distributed throughout the neocortex, basal ganglia, and brainstem. A genome-wide association study identified EIF2AK3 as a risk factor for PSP. EIF2AK3 encodes PERK, part of the endoplasmic reticulum’s (ER) unfolded protein response (UPR). PERK is an ER membrane protein that senses unfolded protein accumulation within the ER lumen. Recently, several groups noted UPR activation in Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis, multiple system atrophy, and in the hippocampus and substantia nigra of PSP subjects. Here, we evaluate UPR PERK activation in the pons, medulla, midbrain, hippocampus, frontal cortex and cerebellum in subjects with PSP, AD, and in normal controls. Results: We found UPR activation primarily in disease-affected brain regions in both disorders. In PSP, the UPR was primarily activated in the pons and medulla and to a much lesser extent in the hippocampus. In AD, the UPR was extensively activated in the hippocampus. We also observed UPR activation in the hippocampus of some elderly normal controls, severity of which positively correlated with both age and tau pathology but not with Aβ plaque burden. Finally, we evaluated EIF2AK3 coding variants that influence PERK activation. We show that a haplotype associated with increased PERK activation is genetically associated with increased PSP risk. Conclusions: The UPR is activated in disease affected regions in PSP and the genetic evidence shows that this activation increases risk for PSP and is not a protective response.
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There is evidence of a common final way leading to PERK hyperactivation in disease-affected brain regions.
“We have previously referred to these topics, but regardless of the disease-specific aggregate, there is evidence of a kind of common final way leading to PERK hyperactivation in disease-affected brain regions [397].”
From GANAB and N-Glycans Substrates Are Relevant in Human Physiology, Polycystic Pathology and Multiple Sclerosis: A Review (2022) · cites this paper as [397]
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- Authors
- Stutzbach, L. D., Xie, S. X., Naj, A. C., Albin, R., Gilman, S., PSP Genetics Study Group, Lee, V. M. Y., Trojanowski, J. Q., Devlin, B., & Schellenberg, G. D.
- Affiliations
- University of Pennsylvania (US)
- University of Michigan (US)
- University of Pittsburgh (US)
- Corresponding author
- Schellenberg, Gerard D
- ORCID
- Venue
- Acta Neuropathologica Communications
- Published
- 2013-07-06
- Volume
- 1
- Issue
- 1
- Pages
- 31-31
- ISSN
- 2051-5960 (ISSN-L)
- PMC
- PMC3893579
- OpenAlex
- W2106758408
- Cited by
- 197
- References
- 59
- Citations by year
- 2026: 10 · 2025: 9 · 2024: 17 · 2023: 23 · 2022: 20 · 2021: 11 · 2020: 34 · 2019: 14 · 2018: 16 · 2017: 14 · 2016: 10 · 2015: 10 · 2014: 8 · 2013: 1
- FWCI
- 5.61
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Acta Neuropathologica Communications (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- D-Scholarship@Pitt (University of Pittsburgh) (acceptedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- Michael J. Fox Foundation for Parkinson's Research (U24 NS072026, 05-901, 211002, P30 AG19610)
- University of Michigan
- Arizona Department of Health Services (P30 AG19610, U24 NS072026, 05-901, 211002, Contract 211002)
- National Institute for Health and Care Research (NF-SI-0512-10033)
- Arizona Biomedical Research Commission (P30 AG19610, 05–901, Contracts 4001, 0011, 05‐901 and 1001, U24 NS072026, 4001, 0011, 05-901, and 1001, 211002)
- National Institutes of Health (U24NS07-2026, 05-901, AG 10 124, 1f31ag043254-01, 211002, AG19610, AG017586)
- National Institute on Aging (211002, P30-AG-19610, F31 AG043254, 1F31AG043254, P50AG005131, AG-19610, P30AG010124, P01AG017586, R37AG011762, AG-10124, R37 AG11762, P30AG019610, 05-901, AG-017586, P50AG005134, P30AG062421)
- National Institute of Neurological Disorders and Stroke (NS072026, 211002, U24NS072026, 05-901, P30 AG19610)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Keywords
- unfolded protein response, PERK, progressive supranuclear palsy, Alzheimer's disease, tau pathology, endoplasmic reticulum stress, passive optical networks, medulla, hippocampus, genetic risk, amyloid plaques
- MeSH terms
- Aged, Aging, Alzheimer Disease, Brain, Female, Haplotypes, Humans, Male, Middle Aged, Supranuclear Palsy, Progressive, tau Proteins, eIF-2 Kinase, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, Unfolded Protein Response
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