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| Home > Publications Database > Elevated CSF GAP-43 is associated with accelerated tau accumulation and spread in Alzheimer's disease. > print |
| 001 | 266772 | ||
| 005 | 20240121002237.0 | ||
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| 024 | 7 | _ | |a 10.1038/s41467-023-44374-w |2 doi |
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| 037 | _ | _ | |a DZNE-2024-00035 |
| 041 | _ | _ | |a English |
| 082 | _ | _ | |a 500 |
| 100 | 1 | _ | |a Franzmeier, Nicolai |0 0000-0001-9736-2283 |b 0 |
| 245 | _ | _ | |a Elevated CSF GAP-43 is associated with accelerated tau accumulation and spread in Alzheimer's disease. |
| 260 | _ | _ | |a [London] |c 2024 |b Nature Publishing Group UK |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1705491120_18421 |2 PUB:(DE-HGF) |
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| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 520 | _ | _ | |a In Alzheimer's disease, amyloid-beta (Aβ) triggers the trans-synaptic spread of tau pathology, and aberrant synaptic activity has been shown to promote tau spreading. Aβ induces aberrant synaptic activity, manifesting in increases in the presynaptic growth-associated protein 43 (GAP-43), which is closely involved in synaptic activity and plasticity. We therefore tested whether Aβ-related GAP-43 increases, as a marker of synaptic changes, drive tau spreading in 93 patients across the aging and Alzheimer's spectrum with available CSF GAP-43, amyloid-PET and longitudinal tau-PET assessments. We found that (1) higher GAP-43 was associated with faster Aβ-related tau accumulation, specifically in brain regions connected closest to subject-specific tau epicenters and (2) that higher GAP-43 strengthened the association between Aβ and connectivity-associated tau spread. This suggests that GAP-43-related synaptic changes are linked to faster Aβ-related tau spread across connected regions and that synapses could be key targets for preventing tau spreading in Alzheimer's disease. |
| 536 | _ | _ | |a 353 - Clinical and Health Care Research (POF4-353) |0 G:(DE-HGF)POF4-353 |c POF4-353 |f POF IV |x 0 |
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| 650 | _ | 7 | |a GAP-43 Protein |2 NLM Chemicals |
| 650 | _ | 7 | |a tau Proteins |2 NLM Chemicals |
| 650 | _ | 7 | |a Amyloid beta-Peptides |2 NLM Chemicals |
| 650 | _ | 7 | |a Biomarkers |2 NLM Chemicals |
| 650 | _ | 2 | |a Humans |2 MeSH |
| 650 | _ | 2 | |a Alzheimer Disease: metabolism |2 MeSH |
| 650 | _ | 2 | |a GAP-43 Protein: genetics |2 MeSH |
| 650 | _ | 2 | |a GAP-43 Protein: metabolism |2 MeSH |
| 650 | _ | 2 | |a tau Proteins: metabolism |2 MeSH |
| 650 | _ | 2 | |a Amyloid beta-Peptides: metabolism |2 MeSH |
| 650 | _ | 2 | |a Brain: metabolism |2 MeSH |
| 650 | _ | 2 | |a Positron-Emission Tomography |2 MeSH |
| 650 | _ | 2 | |a Cognitive Dysfunction: metabolism |2 MeSH |
| 650 | _ | 2 | |a Biomarkers: metabolism |2 MeSH |
| 700 | 1 | _ | |a Dehsarvi, Amir |0 0000-0001-7116-9741 |b 1 |
| 700 | 1 | _ | |a Steward, Anna |b 2 |
| 700 | 1 | _ | |a Biel, Davina |b 3 |
| 700 | 1 | _ | |a Dewenter, Anna |0 0000-0002-5636-196X |b 4 |
| 700 | 1 | _ | |a Roemer, Sebastian Niclas |0 0000-0003-3423-457X |b 5 |
| 700 | 1 | _ | |a Wagner, Fabian |b 6 |
| 700 | 1 | _ | |a Groß, Mattes |b 7 |
| 700 | 1 | _ | |a Brendel, Matthias |0 P:(DE-2719)9001539 |b 8 |
| 700 | 1 | _ | |a Moscoso, Alexis |0 0000-0003-0170-036X |b 9 |
| 700 | 1 | _ | |a Arunachalam, Prithvi |b 10 |
| 700 | 1 | _ | |a Blennow, Kaj |b 11 |
| 700 | 1 | _ | |a Zetterberg, Henrik |0 0000-0003-3930-4354 |b 12 |
| 700 | 1 | _ | |a Ewers, Michael |0 P:(DE-2719)9000543 |b 13 |
| 700 | 1 | _ | |a Schöll, Michael |0 0000-0001-7800-1781 |b 14 |
| 773 | _ | _ | |a 10.1038/s41467-023-44374-w |g Vol. 15, no. 1, p. 202 |0 PERI:(DE-600)2553671-0 |n 1 |p 202 |t Nature Communications |v 15 |y 2024 |x 2041-1723 |
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