27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Moreover, a theoretical model proposes that frontotemporal dementia manifestations result from a deficit in goal-directed behaviour, which may be related to altered dopamine control of the frontostriatal circuitry. 4 key findings →
Participants: 139 Evidence: low
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Serum beta-synuclein level was progressively increased in the AD continuum across the preclinical, MCI and dementia stages compared with controls and was correlated with serum pTau181 (r=0.710), NfL (r=0.494) and GFAP concentrations (r=0.621, p<0.001 for all). 5 key findings →
Participants: 56 Evidence: moderate
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We found higher lipid droplet accumulation in primary fibroblasts derived from these mice, as well as in the brain of the mutant mice. 5 key findings →
Evidence: low
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They are often found in middle-aged individuals and are associated with a greater risk of stroke and vascular dementia. 5 key findings →
Participants: 1,072 Evidence: low
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Type 2 diabetes mellitus (T2D) and Alzheimer's disease (AD) are two of the most common diseases of aging around the world. 4 key findings →
Evidence: low
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Recent technical advances in peripheral blood analysis have enabled precise quantification of Alzheimer´s Disease (AD) biomarkers in the early stages of the AD continuum, in an economical, non-invasive and safe manner. 4 key findings →
Participants: 329 Evidence: moderate
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Glutamate transporter solute carrier family 1, member 2 (GLT1/EAAT2), a major modulator of glutamate homeostasis in astrocytes, is assessed in post-mortem human brain samples of frontal cortex area 8 in advanced stages of Alzheimer disease (AD) and terminal stages of dementia with Lewy bodies (DLB) in order to gain understanding of astrogliopathy in diseases manifested by dementia. 4 key findings →
Evidence: low
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Pulsatile secretion of gonadotropin-releasing hormone (GnRH) is essential for activating and maintaining the function of the hypothalamic-pituitary-gonadal axis, which controls the onset of puberty and fertility. 2 key findings →
Evidence: low
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Despite the central role attributed to neuroinflammation in the etiology and pathobiology of Alzheimer's disease (AD), the direct link between levels of inflammatory mediators in blood and cerebrospinal fluid (CSF) compartments, as well as their potential implications for AD diagnosis and progression, remains inconclusive. 4 key findings →
Participants: 485 Evidence: low
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Participants' age ranged from 45 to 87, 53% were women, and 26% were diagnosed with dementia (39% AD, 18% Lewy Body and 17% Frontotemporal Dementia; Table 1). 5 key findings →
Design: cross-sectional Participants: 255 Evidence: moderate
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Dream recall status was associated with blood p ‐tau217 levels, APOE ε4 carriage, and future cognitive decline among older individuals cognitively healthy at baseline. 5 key findings →
Design: longitudinal study Evidence: moderate
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Early isolated functional disruptions in salience/visual networks were present in asymptomatic carriers, along with anterior cingulate gray matter reductions. 5 key findings →
Evidence: low
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We found a positive main effect of CSF Aβ42/40 (p = 0.011) and p-tau181 (p = 0.012) on BC of the Dorsal Attention Network (DAN) (Figure 1). 5 key findings →
Design: longitudinal study Evidence: moderate
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Plasma glial fibrillary acidic protein (GFAP) has emerged as a promising biomarker of astrocytic reactivity in preclinical Alzheimer´s Disease (AD). 4 key findings →
Participants: 143 Evidence: low
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Damaging nonsynonymous ABCA1 variants had differential AD risk effects between APOE genotype groups and exhibited interaction effects with APOE ε2 and ε4. 5 key findings →
Evidence: moderate
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In the last decade, an important effort was made in the field of Down syndrome to find new interventions that improve cognition. 1 key finding →
Evidence: low
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AD patients exhibited increased expression of pyroptosis-related genes, supporting the involvement of pyroptosis in neurodegeneration. 5 key findings →
Evidence: low
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Fifty-nine patients fulfilled the inclusion criteria. 5 key findings →
Design: case-control study Evidence: moderate
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Individual cognitive profiles of patients with Parkinson's disease dementia (PDD) are highly heterogeneous, suggesting possible biological subtypes. 1 key finding →
Participants: 50 Evidence: low
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The genetic architecture of sporadic Early-Onset Alzheimer Disease (sEOAD, onset ≤65 years) remains largely unknown. 2 key findings →
Evidence: low
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We estimated the overall concentration (mean standardized values) and principal components (PCs) of the proteomics and lipidomics data independently. 5 key findings →
Participants: 1,372 Evidence: moderate
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Alzheimer's disease (AD) is characterized by a progressive cognitive decline involving a multifactorial pathophysiology, including epigenetic dysregulation. 4 key findings →
Evidence: low
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In total, 24 recommendations were developed covering the research landscape and priorities within research in AD following a possible approval, potential impact on health care systems and diagnostic pathways, and communication to patients about anti-amyloid antibodies. 5 key findings →
Evidence: low
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could serve as potential biomarkers for NAFLD-associated mild cognitive impairment; 3) bacterial metabolic functions involved in sugar degradation and the breakdown of tryptophan and glutamate were downregulated and linked to CXCL13 plasma levels and neuroinflammation; 4) correlations between SCFA concentrations disappeared with liver disease and cognitive impairment. 3 key findings →
Evidence: low
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Oropharyngeal dysphagia (OD) is a highly prevalent geriatric syndrome that remains underdiagnosed and undertreated, often resulting in severe nutritional and respiratory complications with poor clinical outcomes. 5 key findings →
Design: narrative review Evidence: moderate
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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 27,780 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.
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 →