Plasma neurofilament light (NFL) levels may be a marker of neuronal injury. 4 key findings →
Participants: 193 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Plasma neurofilament light (NFL) levels may be a marker of neuronal injury. 4 key findings →
Participants: 193 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cumulative data suggest that neuroinflammation plays a prominent role in Alzheimer's disease (AD) pathogenesis. 4 key findings →
Evidence: low
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In total, 881 (21.6%) participants had ILF and 272 (6.8%) participants developed dementia. 5 key findings →
Participants: 4,072 Evidence: low
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Raw scores were converted to regression‐based Z‐scores and averaged at the domain and overall level. 5 key findings →
Design: cohort study Participants: 320 Evidence: moderate
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A decline in TMT was associated with worse cognitive function, increased cerebral tau deposition and impaired functional performance. 5 key findings →
Participants: 801 Evidence: low
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The PD-MCI nonreversion group had greater p-tau:amyloid beta and t-tau:amyloid beta ratios relative to the PD-MCI reversion group. 4 key findings →
Design: longitudinal study Participants: 430 Evidence: moderate
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Soluble N-ethylmaleimide-sensitive factor attachment proteins receptors (SNARE) proteins, such as VAMP-2 and SNAP-25, are implicated in α-synuclein pathophysiology and CSF levels of these proteins are associated with pathophysiological biomarkers and cognitive decline in Alzheimer’s disease (AD). 5 key findings →
Participants: 62 Evidence: moderate
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The study included 25 patients with iCAA (age, 44±11 years), 31 patients with sCAA (age, 75±5 years), 28 patients with AD (age, 71±8 years) and 30 controls (age, 72±8 years) from 9 case descriptions and 1 cohort study. 5 key findings →
Design: cohort study Participants: 25 Evidence: moderate
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Recent advances in our understanding of non-cell-autonomous mechanisms in neurodegenerative diseases (NDDs) have highlighted microglial dysfunction as a core driver of disease progression. 5 key findings →
Evidence: low
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In AD cases, pTau181 and ApoE4 levels were elevated, and the Aβ1-42/1-40 ratio was reduced. 5 key findings →
Participants: 27 Evidence: low
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Alzheimer disease is associated with a significant decrease in CSF beta-amyloid1-42 levels along with an increase in CSF tau levels.
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Our review supports that biofluid biomarker testing could be cost-effective to diagnose AD. 2 key findings →
Design: systematic-review Evidence: moderate
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They belong to the spectrum of neurodegenerative diseases that result in death or dysfunction of neurons with similarities to Alzheimer disease (AD) but also distinctive differences (reviewed (Canet et al., Front Cell Neurosci 12: 307, 2018)). 3 key findings →
Evidence: low
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In Alzheimer's disease (AD), a single-nucleotide polymorphism in the gene encoding brain-derived neurotrophic factor (BDNF Val66Met ) is associated with worse impact of primary AD pathology (beta-amyloid, Aβ) on neurodegeneration and cognitive decline, rendering BDNF Val66Met an important modulating factor of cognitive impairment in AD. 5 key findings →
Participants: 149 Evidence: low
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Genetic pathways implicated in causing AD are related to altered levels of soluble tau through both Aβ-dependent and Aβ-independent mechanisms, which may have relevance for anti-tau drug development. 3 key findings →
Participants: 751 Evidence: low
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This study failed to find associations of circulating NfL and PGRN levels with frailty among community-dwelling older adults in adjusted analyses. 2 key findings →
Design: cross-sectional Participants: 403 Evidence: low
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The mean subject score of the ADCRP was significantly higher in the A+T+ group compared to each of the other group (all p p > 0.1). 2 key findings →
Participants: 269 Evidence: low
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In MCI reverters, abnormal biomarkers for AD pathology are associated with subsequent decline. 2 key findings →
Participants: 757 Evidence: moderate
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Extant data from in vivo animal models and postmortem studies indicate that Alzheimer's disease (AD) pathology is associated with reduction of the brain antioxidant glutathione (GSH), yet direct clinical evidence has been lacking. 2 key findings →
Evidence: low
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Mild cognitive impairment (MCI) is a nosological entity proposed as an intermediate state between normal aging and dementia. 4 key findings →
Participants: 45 Evidence: low
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The brain is the most cholesterol-rich organ in the human body. 5 key findings →
Participants: 32 Evidence: low
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Adiponectin, an adipocytokine released by the adipose tissue and has important roles in the metabolic regulation and inflammatory control, may play an important roles in the physiopathology of psychiatric and neurodegenerative disorders. 4 key findings →
Participants: 157 Evidence: moderate
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Progranulin (PGRN) is predominantly expressed by microglia in the brain, and genetic and experimental evidence suggests a critical role in Alzheimer's disease (AD). 4 key findings →
Evidence: low
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There is limited data on cerebrospinal fluid (CSF) biomarkers in sporadic amyloid-β (Aβ) cerebral amyloid angiopathy (CAA). 4 key findings →
Evidence: low
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Currently there are no effective treatments for many neurodegenerative diseases. 4 key findings →
Evidence: moderate
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10 of the 829 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read
This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.
Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.
Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.
See the whole rubric drawn out → — four charts covering all 27,380 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,032 records (3.8% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →