The CAD106 first-in-human study demonstrated a favorable safety profile and promising antibody response. 4 key findings →
Design: open-label trial Participants: 47 Evidence: high
Full summary, score breakdown and related studies → Original source
Research
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
We sought to identify cognitive measures associated with the earliest detectable signs of emerging Aβ and tau pathology. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Preclinical evidence in transgenic models of Alzheimer's disease suggests that liraglutide exerts neuroprotective effects by reducing amyloid oligomers, normalising synaptic plasticity and cerebral glucose uptake, and increasing the proliferation of neuronal progenitor cells. 4 key findings →
Participants: 206 Evidence: high
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) pathology is thought to progress from normal cognition through preclinical disease and ultimately to symptomatic AD with cognitive impairment. 3 key findings →
Design: cross-sectional Participants: 164 Evidence: moderate
Full summary, score breakdown and related studies → Original source
59/100
In this study, levels of total A(beta)x-40 and A(beta)x-42 were elevated early in dementia and levels of both peptides were strongly correlated with cognitive decline. 4 key findings →
Design: cross-sectional Participants: 16 Evidence: low
Full summary, score breakdown and related studies → Original source
Dysregulated microglia activation, leading to neuroinflammation, is crucial in neurodegenerative disease development and progression. 1 key finding →
Participants: 90,716 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's Disease (AD) is a progressive neurodegenerative disease and the leading cause of dementia. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The global rise in both metabolic syndrome (MetS) and neurodegenerative diseases (NDs), particularly dementia and Alzheimer's disease (AD) poses a growing health and socioeconomic burden. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Higher synaptic latent factor (β = - 0.019, pFDR = 0.021) and YKL-40 (β = - 0.020, pFDR = 0.025) significantly predicted hippocampal atrophy. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The microbiota-gut-brain axis (MGBA) is an intricate bidirectional communication network that links intestinal microbiota with the central nervous system (CNS) through immune, neural, endocrine, and metabolic pathways. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Epidemiologic studies have reported that cancer survivors have a relatively low risk of developing dementia, but the mechanisms underlying that inverse relationship are mostly unknown. 4 key findings →
Participants: 8,121 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The TMEM106B risk variant was significantly enriched in AD cases with transactive response DNA-binding protein 43 kDa (TDP-43) pathology - associating with increased odds of developing AD TDP-43 subtype α - but failed to associate with Lewy body or vascular pathology. 3 key findings →
Participants: 2,604 Evidence: low
Full summary, score breakdown and related studies → Original source
Brain amyloid deposition is thought to be a seminal event in Alzheimer’s disease. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Brain degeneration in patients with Alzheimer's disease (AD) results from the accumulation of pathological amyloid- (Aβ) plaques and tau protein tangles, leading to altered plasma levels of biomarkers. 5 key findings →
Design: cross-sectional Participants: 40 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Little is known whether cerebrospinal fluid (CSF) biomarkers of Alzheimer's disease (AD) can predict both memory decline and associated longitudinal medial temporal lobe (MTL) gray matter (GM) reductions in cognitively healthy individuals. 2 key findings →
Design: longitudinal study Participants: 57 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Amyloid, tau, neurodegeneration and neuroinflammation plasma biomarkers are modified in DLB, albeit with moderate diagnosis performance. 2 key findings →
Participants: 104 Evidence: low
Full summary, score breakdown and related studies → Original source
Lumipulse plasma Aβ 42 /Aβ 40 is a scalable assay for detection of cerebral Aβ and prediction of risk for cognitive decline across the AD continuum. 2 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Serum Abeta40/42 ratio was significantly higher in MDD patients than in controls, and this difference was seen for both elderly and young subjects. 5 key findings →
Design: cohort study Participants: 60 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Exposure to environmental chemicals such as lead (Pb) during vulnerable developmental periods can result in adverse health outcomes later in life. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
We identified a series of transmembrane proteins, proteins associated with or anchored to the plasma membrane, and proteins involved in or connected to synaptic vesicle transport to be associated with CSF biomarkers of amyloid and tau pathology in AD. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The evaluation of blood biomarkers on an automated platform exhibited high diagnostic accuracy for AD pathophysiology, and pTau 217 showed excellent diagnostic accuracy to identify participants with AD in a consecutive sample representing the routine clinical practice in a specialized memory unit. 1 key finding →
Participants: 130 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
CSF synaptic biomarkers increase in the early preclinical stages of the Alzheimer continuum even when a low burden of Aβ pathology is present, and they differ in their association with age, sex, APOE ε4 , and markers of neurodegeneration. 4 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
While plasma biomarkers for Alzheimer's disease (AD) are increasingly being evaluated for clinical diagnosis and prognosis, few population-based autopsy studies have evaluated their utility in the context of predicting neuropathological changes. 3 key findings →
Participants: 350 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Apolipoprotein E is immunochemically localized to the senile plaques, vascular amyloid, and neurofibrillary tangles of Alzheimer disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Elderly patients with diabetes develop more extensive vascular pathology, which alone or together with AD-type pathology (particularly in APOE ε4 carriers) results in increased dementia risk. 2 key findings →
Participants: 553 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
From across this tag
10 of the 6,970 studies in this tag that have a study page, 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.
- Protective or Pathogenic? Microglial Responses at the Intersection of Amyloid-β, Tau, and Neuroinflammation in Alzheimer’s Disease
- Alterations in glia and axons in the brains of Binswanger's disease patients
- Amyloid-β42/40 ratio drives tau pathology in 3D human neural cell culture models of Alzheimer's disease
- Amyloid-β protein oligomerization and the importance of tetramers and dodecamers in the aetiology of Alzheimer's disease
- Beneficial effects of natural flavonoids on neuroinflammation
- Oxidative stress and metabolic syndrome
- Corticostriatal synaptic function in mouse models of Huntington's disease: early effects of huntingtin repeat length and protein load
- Neuroinflammation and Tauopathies
- Endogenous brain cytokine mRNA and inflammatory responses to lipopolysaccharide are elevated in the Tg2576 transgenic mouse model of Alzheimer's disease
- Clinical criteria for limbic-predominant age-related TDP-43 encephalopathy
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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →