Alzheimer's disease (AD) is strongly associated with microglia-induced neuroinflammation. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Cerebrospinal fluid (CSF) concentrations of amyloid-beta (Abeta) 1-38, 1-40, 1-42, total-tau and phospho-tau in samples from 156 patients with Alzheimer's disease (AD) (n = 44), depressive cognitive complainers (DCC, n = 25) and various other forms of non-Alzheimer dementias (NAD, n = 87) were analyzed by electrochemiluminescence and enzyme linked immunosorbent assay, respectively. 4 key findings →
Participants: 44 Evidence: low
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Microglial activation is a key feature in Alzheimer's disease and is considered to contribute to progressive neuronal injury by release of neurotoxic products. 4 key findings →
Evidence: low
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Our findings support speech-based cognitive assessments as a promising avenue towards remote MCI screening, with implications for scalable screening in clinical trials and healthcare. 3 key findings →
Participants: 110 Evidence: low
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Increased peripheral and central nervous system cortisol levels have been reported in Alzheimer's disease (AD) and may reflect dysfunction of cerebral components of the hypothalamic-pituitary-adrenal (HPA) axis. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is an irreversible, devastating neurodegenerative brain disorder characterized by the loss of neurons and subsequent cognitive decline. 4 key findings →
Evidence: low
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The findings of this study are consistent with previous reports demonstrating a high aggregation propensity of Aβ 4-x peptides and suggest an important role of these N-truncated Aβ species in the process of amyloidogenesis and plaque core formation. 1 key finding →
Evidence: low
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The amyloid precursor protein (APP) is implied both in cell growth and differentiation and in neurodegenerative processes in Alzheimer disease. 4 key findings →
Evidence: low
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Across both regions, no evidence of reduced total neuronal density was observed, but a modest reduction in parvalbumin interneurons was observed in the cingulate gyrus, and there were only modest reductions in some synaptic markers in DLB. 4 key findings →
Participants: 20 Evidence: low
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The beta-amyloid precursor protein (APP) represents a type I transmembrane glycoprotein that is ubiquitously expressed. 4 key findings →
Evidence: low
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Frontotemporal dementia is a debilitating neurodegenerative disorder characterized by frontal and temporal lobe degeneration, resulting in behavioral changes, language difficulties, and cognitive decline. 2 key findings →
Evidence: low
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Neural autoantibodies are being increasingly detected in conjunction with neurodegenerative dementias such as Alzheimer's disease dementia (AD), yet their significance is not well clarified. 4 key findings →
Design: case report Evidence: low
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HEK293, Neuro2a and SH-SY5Y expressing increased levels of α-synuclein were treated with sonicated α-synuclein pre-formed fibrils, to model seeded aggregation. 1 key finding →
Evidence: low
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The study highlights the potential of integrating 18 F-FDG-PET with CSF biomarkers to improve the diagnosis, prognosis, and monitoring of AD, emphasizing the complexity and regional specificity of biomarker interactions in neurodegeneration. 1 key finding →
Participants: 90 Evidence: moderate
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In older adults, temporal [18F]PI-2620 binding was higher in women (β = 0.543, P < 0.001) and APOE4 carriers (β = 0.395, P = 0.030) and was positively associated with plasma p-tau217 (β = 0.22, P = 0.008). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
40/100
High Resolution Image Download MS PowerPoint Slide The aggregation of α-synuclein is crucial to the development of Lewy body diseases, including Parkinson’s disease and dementia with Lewy bodies. 1 key finding →
Evidence: low
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Only FCSRT-IR LTR rates sufficiently differentiated SCD from HC (AUC of 0.701; 95% CI 0.537-0.865). 4 key findings →
Evidence: low
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Successful back-translating clinical biomarkers and molecular imaging methods of Alzheimer's disease (AD), including positron emission tomography (PET), are very valuable for the evaluation of new therapeutic strategies and increase the quality of preclinical studies. 18 F-Fluorodeoxyglucose (FDG)-PET and 18 F-Florbetaben-PET are clinically established biomarkers capturing two key pathological features of AD. 3 key findings →
Evidence: low
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Interprofessional case conferences may lead to more awareness regarding gaps in primary palliative care, one's own care routines or a lack of psychosocial support. 5 key findings →
Evidence: high
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The primary analysis demonstrated significant improvements in multiple episodic memory measures across both intervention groups, with no significant differences observed between groups. 5 key findings →
Design: post-hoc analysis Evidence: low
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Lewy body dementias (LBD), comprising dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD), are defined by misfolded α-synuclein aggregation. 1 key finding →
Evidence: low
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Autoantibody-associated psychiatric syndromes are a novel disease entity that is not fully understood. 4 key findings →
Evidence: moderate
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Dementias are expensive diseases: the net annual cost in European healthcare is about € 28.000 per case with a strong stage dependency, of which medical care accounts for about 19%. 2 key findings →
Evidence: low
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In accordance with the current German dementia guidelines, the dementia biomarkers amyloid beta 42, the tau peptides total tau and phosphorylated tau 181 are recommended for cerebrospinal fluid (CSF)-based diagnostics of dementia. 3 key findings →
Evidence: low
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BackgroundThe brain age gap (BAG), the difference between neuroimaging-predicted and chronological age, captures inter-individual variation in brain aging. 2 key findings →
Design: longitudinal study Participants: 202 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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 27,780 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.
What this library is — and isn't
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.
1,034 records (3.7% 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 →