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48/100

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Risk factors

Topic: Amyloid, tau and blood-test diagnosis

The Alzheimer's disease (AD) afflicted brain is neuropathologically defined by extracellular amyloid-β (Aβ) plaques and intraneuronal neurofibrillary tangles composed of hyperphosphorylated tau protein. However, accumulating evidence suggests that the presynaptic protein α-synuclein (αSyn), mainly associated with synucleinopathies like Parkinson's disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy (MSA), is involved in the pathophysiology of AD. Lewy-related pathology (LRP), primarily comprised of αSyn, is present in a majority of autopsied AD brains, and higher levels of αSyn in the cerebrospinal fluid (CSF) of patients with mild cognitive impairment (MCI) and AD have been linked to cognitive decline. Recent studies also suggest that the asymptomatic accumulation of Aβ plaques is associated with higher CSF αSyn levels in subjects at risk of sporadic AD and in individuals carrying autosomal dominant AD mutations. Experimental evidence has further linked αSyn mainly to tau hyperphosphorylation, but also to the pathological actions of Aβ and the APOEε4 allele, the latter being a major genetic risk factor for both AD and DLB. In this review, we provide a summary of the current evidence proposing an involvement of αSyn either as an active or passive player in the pathophysiological ensemble of AD, and furthermore describe in detail the current knowledge of αSyn structure and inferred function.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Twohig, D., & Nielsen, H. M. (2019). α-synuclein in the pathophysiology of Alzheimer's disease. Molecular neurodegeneration. https://doi.org/10.1186/s13024-019-0320-x

Vancouver

Twohig D, Nielsen HM. α-synuclein in the pathophysiology of Alzheimer's disease. Molecular neurodegeneration. 2019. doi:10.1186/s13024-019-0320-x. PMID: 31186026.

BibTeX

@article{twohig2019-31186026,
  author  = {Twohig, D. and Nielsen, H. M.},
  title   = {{α-synuclein in the pathophysiology of Alzheimer's disease}},
  journal = {Molecular neurodegeneration},
  year    = {2019},
  doi     = {10.1186/s13024-019-0320-x},
  pmid    = {31186026},
  url     = {https://doi.org/10.1186/s13024-019-0320-x}
}

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Key findings

However, accumulating evidence suggests that the presynaptic protein α-synuclein (αSyn), mainly associated with synucleinopathies like Parkinson's disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy (MSA), is involved in the pathophysiology of AD.
Recent studies also suggest that the asymptomatic accumulation of Aβ plaques is associated with higher CSF αSyn levels in subjects at risk of sporadic AD and in individuals carrying autosomal dominant AD mutations.

Why it matters

This review summarizes evidence that the protein alpha-synuclein is involved in the pathophysiology of Alzheimer's disease and that higher cerebrospinal fluid alpha-synuclein levels have been linked to cognitive decline. It is a review of mechanisms and biomarkers, not a treatment or prevention trial.

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Study details

Evidence strengthLow

How this study scored 48/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Molecular neurodegeneration)
Journal's citation record	2 / 4	Molecular Neurodegeneration: journal h-index 164 (OpenAlex, 2026-10-29)
Study design	0 / 12	No study design recorded — scores zero, not guessed (not stated in the record — scored 0)
Strength of evidence	1 / 5	Rated “low” in our summary
Peer-review validation	10 / 10	Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent	2 / 5	2019 — within 10 year(s) of the newest study here
Sample size	0 / 4	Participant count not stated — scores zero (not stated in the record — scored 0)
Effect reported	0 / 3	No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people	0 / 3	Not stated whether this was studied in people — scores zero (not stated in the record — scored 0)
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	6 / 7	Cited 373 times (OpenAlex, 2026-10-10)
Citations per year	4 / 5	41.4 citations a year over 9 year(s) since 2019
Impact for its field and year	4 / 6	Cited 17.5× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	2 / 6	Cited by 9 other studies in this library
Still being cited	3 / 4	Cited 188 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	2 / 4	Last-listed author Henrietta M. Nielsen: h-index 30 (OpenAlex, whole career)
Institution's track record	1 / 3	Stockholm University: institution h-index 972 (OpenAlex)
Multicenter collaboration	0 / 3	OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete)
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 31186026)
Free to read	2 / 2	Free to read
Total	48 / 100	—

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