The relevance of cerebrospinal fluid α-synuclein levels to sporadic and familial Alzheimer’s disease
Open accessAbstract
Accumulating evidence demonstrating higher cerebrospinal fluid (CSF) α-synuclein (αSyn) levels and αSyn pathology in the brains of Alzheimer’s disease (AD) patients suggests that αSyn is involved in the pathophysiology of AD. To investigate whether αSyn could be related to specific aspects of the pathophysiology present in both sporadic and familial disease, we quantified CSF levels of αSyn and assessed links to various disease parameters in a longitudinally followed cohort (n = 136) including patients with sporadic mild cognitive impairment (MCI) and AD, and in a cross-sectional sample from the Dominantly Inherited Alzheimer’s Network (n = 142) including participants carrying autosomal dominant AD (ADAD) gene mutations and their non-mutation carrying family members. Our results show that sporadic MCI patients that developed AD over a period of two years exhibited higher baseline αSyn levels (p = 0.03), which inversely correlated to their Mini-Mental State Examination scores, compared to cognitively normal controls (p = 0.02). In the same patients, there was a dose-dependent positive association between CSF αSyn and the APOEε4 allele. Further, CSF αSyn levels were higher in symptomatic ADAD mutation carriers versus non-mutation carriers (p = 0.03), and positively correlated to the estimated years from symptom onset (p = 0.05) across all mutation carriers. In asymptomatic (Clinical Dementia Rating < 0.5) PET amyloid-positive ADAD mutation carriers CSF αSyn was positively correlated to 11C-Pittsburgh Compound-B (PiB) retention in several brain regions including the posterior cingulate, superior temporal and frontal cortical areas. Importantly, APOEε4-positive ADAD mutation carriers exhibited an association between CSF αSyn levels and mean cortical PiB retention (p = 0.032). In both the sporadic AD and ADAD cohorts we found several associations predominantly between CSF levels of αSyn, tau and amyloid-β1–40. Our results suggest that higher CSF αSyn levels are linked to AD pathophysiology at the early stages of disease development and to the onset of cognitive symptoms in both sporadic and autosomal dominant AD. We conclude that APOEε4 may promote the processes driven by αSyn, which in turn may reflect on molecular mechanisms linked to the asymptomatic build-up of amyloid plaque burden in brain regions involved in the early stages of AD development.
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A recent study described a novel link between the APOEε4 risk allele, cerebrospinal fluid αSyn levels and amyloid-β deposition at the very early stages of Alzheimer's disease development.
“our recent study described a novel link between the APOEε4 risk allele, CSF αSyn levels and Aβ deposition at the very early stages of AD development [27].”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [27]
In ADAD, asymptomatic and APOEε4 positive mutation carriers have a significant positive association between increased CSF αSyn levels and brain Aβ deposition in regions known to exhibit early Aβ deposition.
“asymptomatic ADAD mutation carriers, and APOEε4 positive ADAD mutation carriers had significant positive association between increased CSF αSyn levels and brain Aβ deposition in regions know to exhibit early Aβ deposition”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as Twohig et al. 2018 [27]
In MCI-AD patients, CSF αSyn levels show a positive dose-dependent association with the APOEε4 allele.
“MCI-AD patients also exhibited a positive dose-dependent association between CSF αSyn levels and the APOEε4 allele”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as Twohig et al. 2018 [27]
CSF αSyn levels are higher in symptomatic ADAD mutation carriers than in asymptomatic ADAD mutation carriers.
“CSF αSyn levels were higher in symptomatic ADAD mutation carriers versus asymptomatic ADAD mutation carriers”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as Twohig et al. 2018 [27]
In sporadic AD, baseline CSF αSyn levels are increased in MCI patients who convert to AD after two years.
“at baseline CSF αSyn levels were increased in MCI patients who converted to AD after two years (MCI-AD)”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as Twohig et al. 2018 [27]
In a cross-sectional sample of autosomal dominant Alzheimer's disease mutation carriers from the Dominantly Inherited Alzheimer Network, cerebrospinal fluid αSyn levels were significantly correlated to the estimated years from disease onset.
“in a cross-sectional sample of participants carrying ADAD mutations from the Dominantly Inherited Alzheimer Network (DIAN) we found that CSF αSyn levels were significantly correlated to the estimated years from disease onset [27].”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [27]
In asymptomatic (CDR<0.5) Dominantly Inherited Alzheimer Network participants who carried autosomal dominant Alzheimer's disease mutations and were APOEε4 positive, higher cerebrospinal fluid αSyn levels significantly correlated to PiB-PET amyloid-β plaque burden in several early amyloid-β-accumulating brain areas.
“specifically in asymptomatic (CDR<0.5) DIAN participants who carried ADAD mutations and who also were APOEε4 positive, higher CSF αSyn levels significantly correlated to PiB-PET Aβ plaque burden in several of the ‘early Aβ-accumulating brain areas’.”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [27]
In the authors' study, there were no significant correlations between cerebrospinal fluid αSyn and amyloid-β1-42.
“we, rather unexpectedly, failed to record any significant correlations between CSF αSyn and Aβ1-42 [27].”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [27]
Numerous studies have documented unaltered or slightly increased cerebrospinal fluid αSyn levels in patients with mild cognitive impairment and Alzheimer's disease.
“numerous studies have documented unaltered or slightly increased CSF αSyn levels in patients with MCI and AD [27, 80–82, 86, 90, 91, 93, 94].”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [27]
CSF αSyn levels positively correlate with estimated years from symptom onset in ADAD mutation carriers.
“CSF αSyn levels positively correlated with estimated years from symptom onset in ADAD mutation carriers”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as Twohig et al. 2018 [27]
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Self-citationCerebrospinal fluid α‐synuclein levels in Parkinson's disease – changed or unchanged?
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The probabilistic model of Alzheimer disease: the amyloid hypothesis revised
Frisoni, G. B., Altomare, D., Thal, D. R., Ribaldi, F., van der Kant, R., Ossenkoppele, R., Blennow, K., Cummings, J., van Duijn, C., Nilsson, P. M., et al. (2022) · Nature Reviews Neuroscience · doi:10.1038/s41583-021-00533-w · Cited by 513 · see citing works
α-synuclein in the pathophysiology of Alzheimer’s disease
Twohig, D., & Nielsen, H. M. (2019) · Molecular Neurodegeneration · doi:10.1186/s13024-019-0320-x · Cited by 374 · see citing works
“…• CSF αSyn levels were positively correlated with t-tau in non-mutation and ADAD mutation carriers, and with p-tau in non-mutation carriers and PSEN1 mutation carriers only (not APP or PSEN2 mutation carriers) • Twohig et al. 2018 [27] AD Alzheimer’s disease, DLB dementia with Lewy bodies, PD…”
BackgroundResultInfluentialSelf-citationFernández-Calle, R., Konings, S. C., Frontiñán-Rubio, J., García-Revilla, J., Camprubí-Ferrer, L., Svensson, M., Martinson, I., Boza-Serrano, A., Venero, J. L., Nielsen, H. M., et al. (2022) · Molecular Neurodegeneration · doi:10.1186/s13024-022-00566-4 · Cited by 278 · see citing works
Self-citationLate-onset vs nonmendelian early-onset Alzheimer disease
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Cerebrospinal Fluid Biomarkers of Alzheimer’s Disease: Current Evidence and Future Perspectives
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APOE4 exacerbates α-synuclein pathology and related toxicity independent of amyloid
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Self-citationInsulin Resistance Exacerbates Alzheimer Disease via Multiple Mechanisms
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Alpha-synuclein: a pathological factor with Aβ and tau and biomarker in Alzheimer’s disease
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“In addition, the α-syn levels in CSF were elevated in patients who converted from MCI to AD and with a shorter duration of AD progression [78, 95, 115].”
BackgroundResultInfluentialFunctional and Pathological Effects of α-Synuclein on Synaptic SNARE Complexes
Gao, V., Briano, J. A., Komer, L. E., & Burré, J. (2022) · Journal of Molecular Biology · doi:10.1016/j.jmb.2022.167714 · Cited by 96 · see citing works
Immunotherapies for Aging-Related Neurodegenerative Diseases—Emerging Perspectives and New Targets
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Icariin and Its Metabolites as Potential Protective Phytochemicals Against Alzheimer’s Disease
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Update on CSF Biomarkers in Parkinson’s Disease
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“Correlations of the CSF α-syn level with AD markers have been reported [17,18].”
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Neurogranin as a Novel Biomarker in Alzheimer’s Disease
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Potential neuroprotection by Dendrobium nobile Lindl alkaloid in Alzheimer's disease models
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“Furthermore, higher levels of α-syn in the cerebrospinal fluid (CSF) of patients with mild cognitive impairment correlated with higher probability of progression to AD [95].”
BackgroundClinical and diagnostic implications of Alzheimer's disease copathology in Lewy body disease
Barba, L., Abu‐Rumeileh, S., Barthel, H., Massa, F., Foschi, M., Bellomo, G., Gaetani, L., Thal, D. R., Parnetti, L., & Otto, M. (2024) · Brain · doi:10.1093/brain/awae203 · Cited by 48 · see citing works
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“We specifically found that higher CSF α-synuclein levels were linked to Aβ pathology in APOE ε4-carrying subjects with asymptomatic familial AD [45], and to disease progression in sporadic AD patients examined in the current study.”
BackgroundSelf-citationTherapeutic potential of the medicinal mushroom Ganoderma lucidum against Alzheimer's disease
Chen, X.-J., Deng, Z., Zhang, L., Pan, Y., Fu, J., Zou, L., Bai, Z., Xiao, X., & Sheng, F. (2024) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2024.116222 · Cited by 45 · see citing works
Myelin dysfunction in aging and brain disorders: mechanisms and therapeutic opportunities
Huang, Z., Zhang, Y., Zou, P., Zong, X., & Zhang, Q. (2025) · Molecular Neurodegeneration · doi:10.1186/s13024-025-00861-w · Cited by 46 · see citing works
Novel blood test for early biomarkers of preeclampsia and Alzheimer’s disease
Cheng, S., Banerjee, S., Daiello, L. A., Nakashima, A., Jash, S., Huang, Z., Drake, J., Ernerudh, J., Berg, G. E., Padbury, J. F., et al. (2021) · Scientific Reports · doi:10.1038/s41598-021-95611-5 · Cited by 41 · see citing works
Biomarkers: Our Path Towards a Cure for Alzheimer Disease
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Cerebrospinal fluid biomarkers of Alzheimer's disease in a cohort of adults with Down syndrome
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“Aluminum-induced AD is a widely used animalmodel for studying the pathogenesis of AD.25,26 To date, there is no effective therapeutic intervention in the treatment of AD.27 The present study is a trial to re-purpose the previously used drugs to be a new approach to cut the pathophysiology of AD.”
BackgroundInfluentialData-mining-based biomarker evaluation and experimental validation of SHTN1 for bladder cancer
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Alzheimer’s Disease Biomarker Detection Using Field Effect Transistor-Based Biosensor
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Fluid Candidate Biomarkers for Alzheimer’s Disease: A Precision Medicine Approach
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“VILIP-1 is a neuronal calcium sensor protein involved in signaling pathways related to synaptic plasticity [231].”
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A manifesto for Alzheimer’s disease drug discovery in the era of disease-modifying therapies
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“Moreover, elevated levels of total ⍺ Syn in CSF have been detected in several AD cohorts, including a pre-symptomatic cohort of patients with familial forms of AD [144, 145].”
Associations Between APOE Variants, Tau and α-Synuclein
Rodriguez‐Vieitez, E., & Nielsen, H. M. (2019) · Advances in experimental medicine and biology · doi:10.1007/978-981-32-9358-8_15 · Cited by 24 · see citing works
Self-citationPlasma Apolipoprotein E Monomer and Dimer Profile and Relevance to Alzheimer’s Disease
Patra, K., Giannisis, A., Edlund, A. K., Sando, S. B., Lauridsen, C., Berge, G., Grøntvedt, G. R., Bråthen, G., White, L. R., & Nielsen, H. M. (2019) · Journal of Alzheimer's Disease · doi:10.3233/jad-190175 · Cited by 22 · see citing works
Self-citationKhedher, M. R. B., Haddad, M., Laurin, D., & Ramassamy, C. (2021) · Alzheimer s & Dementia Translational Research & Clinical Interventions · doi:10.1002/trc2.12124 · Cited by 21 · see citing works
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“Additionally, α -syn is associated with Tau hyperphosphorylation and the pathological effects of A β [33–35].”
BackgroundIbáñez, L., Bahena, J. A., Yang, C., Dube, U., Farias, F., Budde, J., Bergmann, K., Brenner-Webster, C., Morris, J. C., Perrin, R. J., et al. (2020) · Acta Neuropathologica Communications · doi:10.1186/s40478-020-01072-8 · Cited by 20 · see citing works
Self-citationα-Synuclein Heteromers in Red Blood Cells of Alzheimer’s Disease and Lewy Body Dementia Patients
Daniele, S., Baldacci, F., Piccarducci, R., Palermo, G., Giampietri, L., Manca, M. L., Pietrobono, D., Frosini, D., Nicoletti, V., Tognoni, G., et al. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-201038 · Cited by 19 · see citing works
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“Increased cerebrospinal fluid ASYN levels is correlated with disease progression from mild cognitive impairment (MCI) to AD (Berge et al., 2016; Twohig et al., 2018) and inversely correlated with cognitive function as measured by Mini-Mental State Exam (MMSE) scores (Korff et al., 2013; Majbour et…”
Piccoli, T., Blandino, V., Maniscalco, L., Matranga, D., Graziano, F., Guajana, F., Agnello, L., Sasso, B. L., Gambino, C. M., Giglio, R. V., et al. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms231810831 · Cited by 16 · see citing works
“α-Syn has already been associated with AD pathology, and aggregates were found in patients affected by AD [29,37,44,45,49,57,68,69], but the ratio has never been tested before.”
BackgroundNeubauer, A., Weissenbrunner, D., Pekrun, S., Roeber, S., Ruf, V. C., Feyen, P. L. C., Strübing, F., & Herms, J. (2025) · Acta Neuropathologica · doi:10.1007/s00401-025-02952-w · Cited by 17 · see citing works
“ApoE4 is also a risk factor for DLB [12] and increased α-syn levels in the cerebrospinal fluid of AD patients [75].”
Zúñiga, C. H., Gallo, B. I. A., Menchaca, R., Amescua, C. A., Hong, S. S., Hui, L., Gil, M., Rhee, Y., Yoon, S., Kim, M., et al. (2025) · Alzheimer s Research & Therapy · doi:10.1186/s13195-025-01681-2 · Cited by 15 · see citing works
“Lewy-related pathology (LRP), primarily comprised of α-syn, is present in a majority of autopsied AD brains, and higher levels of α-syn in the cerebrospinal fluid (CSF) of patients with mild cognitive impairment (MCI) and AD have been linked to cognitive decline [56].”
Perni, M., Mannini, B., Xu, C. K., Kumita, J. R., Dobson, C. M., Chiti, F., & Vendruscolo, M. (2021) · Scientific Reports · doi:10.1038/s41598-021-93527-8 · Cited by 14 · see citing works
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Exploring the effect of APOE ε4 on biomarkers of neurodegeneration in Alzheimer’s disease
Agnello, L., Gambino, C. M., Ciaccio, A. M., Piccoli, T., Blandino, V., Scazzone, C., Sasso, B. L., Ben, F. D., & Ciaccio, M. (2024) · Clinica Chimica Acta · doi:10.1016/j.cca.2024.119876 · Cited by 12 · see citing works
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“There are reports about the dose-response relationship between the AD risk increasing allele, APOEε4 , and CSF α-syn levels, with APOEε4 homozygotes having the highest CSF α-syn levels [210].”
Neuropsychiatric symptoms and apolipoprotein E genotypes in neurocognitive disorders
Lozupone, M., Leccisotti, I., Mollica, A., Berardino, G., Moretti, M. C., Altamura, M., Bellomo, A., Daniele, A., Dibello, V., Solfrizzi, V., et al. (2025) · Neural Regeneration Research · doi:10.4103/nrr.nrr-d-24-01274 · Cited by 11 · see citing works
“Interestingly, in AD patients, the APOE ε4 allele has been associated with higher cerebrospinal fluid (CSF) α-syn levels, particularly in those with MCI who later progressed to AD, showing a dose-dependent effect of the APOE ε4 allele (Twohig, 2018).”
15 years of longitudinal genetic, clinical, cognitive, imaging, and biochemical measures in DIAN
Daniels, A. J., McDade, E., Llibre-Guerra, J., Xiong, C.-J., Perrin, R., Ibanez, L., Supnet-Bell, C., Cruchaga, C., Goate, A., Renton, A. E., et al. (2026) · npj Dementia · doi:10.1038/s44400-025-00047-7 · Cited by 2 · see citing works
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“Similarly, elevated levels of soluble α-synuclein are observed in the cerebral spinal fluid of patients with Alzheimer’s disease [31] and mild cognitive impairment [32,33] relative to controls.”
BackgroundDing, Y., Wang, L., Liu, J., Deng, Y., Jiao, Y., & Zhao, A. (2025) · The Journal of Prevention of Alzheimer s Disease · doi:10.1016/j.tjpad.2024.100040 · Cited by 8 · see citing works
Beyond amyloid plaque, targeting α-synuclein in Alzheimer disease: The battle continues
Al-Kuraishy, H. M., Sulaiman, G. M., Mohammed, H. A., Al-Gareeb, A. I., Albuhadily, A. K., Ali, A. A., & Abu-Alghayth, M. H. (2025) · Ageing Research Reviews · doi:10.1016/j.arr.2025.102684 · Cited by 10 · see citing works
Lucena, D. D., Escaramís, G., Villar‐Piqué, A., Hermann, P., Schmitz, M., Varges, D., Santana, I. J., del Rı́o, J. A., Martı́, E., Ferrer, I., et al. (2020) · Journal of Neurology · doi:10.1007/s00415-020-09870-9 · Cited by 8 · see citing works
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Validity of CSF alpha-synuclein to predict psychosis in prodromal Alzheimer's disease
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“A number of studies have reported AS pathology in approximately 50% of autopsied patients with AD (25, 36).”
BackgroundPostencephalitic Parkinsonism: Unique Pathological and Clinical Features—Preliminary Data
Strobel, S., Sian‐Hülsmann, J., Tappe, D., Jellinger, K. A., Riederer, P. F., & Monoranu, C. (2024) · Cells · doi:10.3390/cells13181511 · Cited by 5 · see citing works
“More importantly, Twohig and colleagues (2018) reported an association between α -synuclein concentration in the cerebrospinal fluid, APOE ε 4 risk allele, and amyloid beta deposits in early AD [61].”
BackgroundCao, T. H. M., Le, A. P. H., Tran, T. T., Huynh, V. K., Pham, B. H., Le, T., Nguyen, Q. L., Tran, T. C., Tong, T. M., Than, T. H. N., et al. (2023) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2023.1308610 · Cited by 3 · see citing works
Staging and markers in Parkinson’s disease and Lewy body disorders: narrative review
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“On the contrary, ApoE2 is a genetic protective factor for Alzheimer’s disease (AD), and its exact mechanism is not yet clear (20).”
Wang, Y.-C., Huang, L.-Y., Yan-Fu, Xiong, S.-Y., Wang, Z.-T., Tan, C., & Tan, L. (2025) · Journal of Translational Medicine · doi:10.1186/s12967-025-06729-3 · Cited by 1 · see citing works
Emerging biomarkers for Parkinson's disease in biological fluids
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Synaptotoxic forms of amyloid-β and α-synuclein act through a common pathwayPreprint
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Ibanez, L., Bahena, J. A., Yang, C., Dube, U., Farias, F. G., Budde, J. P., Bergmann, K., Brenner-Webster, C., Morris, J. C., Perrin, R. J., et al. (2020) · Figshare · doi:10.6084/m9.figshare.13265837
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- Authors
- for the Dominantly Inherited Alzheimer Network (DIAN), Twohig, D., Rodriguez-Vieitez, E., Sando, S. B., Berge, G., Lauridsen, C., Møller, I., Grøntvedt, G. R., Bråthen, G., Patra, K., Bu, G., Benzinger, T. L. S., Karch, C. M., Fagan, A., Morris, J. C., Bateman, R. J., Nordberg, A., White, L. R., & Nielsen, H. M.
- Affiliations
- Stockholm University (SE)
- Norwegian University of Science and Technology (NO)
- St Olav's University Hospital (NO)
- Mayo Clinic (US)
- Washington University in St. Louis (US)
- Karolinska University Hospital (SE)
- Corresponding author
- Nielsen, Henrietta M.
- ORCID
- Venue
- Acta Neuropathologica Communications
- Published
- 2018-11-26
- Volume
- 6
- Issue
- 1
- Pages
- 130-130
- ISSN
- 2051-5960 (ISSN-L)
- PMC
- PMC6260771
- OpenAlex
- W2902816648
- Cited by
- 68
- References
- 68
- Citations by year
- 2026: 3 · 2025: 11 · 2024: 13 · 2023: 6 · 2022: 8 · 2021: 9 · 2020: 14 · 2019: 4
- FWCI
- 4.63
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Acta Neuropathologica Communications (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Digital Commons@Becker (Washington University School of Medicine) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- NORA - Norwegian Open Research Archives (submittedVersion, cc-by)
- Rare & Special e-Zone (The Hong Kong University of Science and Technology) (submittedVersion)
- Funders
- National Institute on Aging (U19AG032438)
- Demensförbundet (2017)
- Alzheimer's Association (2015-NIRG-339824)
- Stiftelsen Olle Engkvist Byggmästare (184-333)
- VINNOVA (2015-04905)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Keywords
- alpha-synuclein, cerebrospinal fluid biomarkers, Alzheimer's disease, sporadic Alzheimer's disease, familial Alzheimer's disease, mild cognitive impairment, APOE ε4, amyloid PET, Pittsburgh compound B, tau protein, amyloid-beta, disease progression, early-stage disease, biomarker discovery
- MeSH terms
- Aged, Alzheimer Disease, Aniline Compounds, Apolipoproteins E, Brain, Cross-Sectional Studies, Female, Humans, Image Processing, Computer-Assisted, Magnetic Resonance Imaging, Male, Middle Aged, Mutation, Peptide Fragments, ROC Curve, Thiazoles, Cohort Studies, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, tau Proteins, Statistics, Nonparametric, Positron-Emission Tomography, alpha-Synuclein, Cognitive Dysfunction
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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