30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The mechanisms responsible for the pathological deposition of brain iron in Parkinson's disease, Alzheimer's disease and other human neurodegenerative disorders remain poorly understood. 2 key findings →
Evidence: low
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Immunocytochemical techniques was used to compare the proportion of neurons expressing various neurotransmitters (tyrosine hydroxylase, choline acetyltransferase and gamma-aminobutyric acid), neuropeptides (Leu-enkephalin and substance P) and neural cell adhesion molecules (NCAM) in the hippocampus, frontal (area 10) and occipital (area 17) cortices of neurologically normal elderly humans to that of age-matched Alzheimer disease (AD) patients. 3 key findings →
Evidence: low
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We recently identified a cDNA encoding a human brain specific trypsinogen (trypsinogen IV). 2 key findings →
Evidence: low
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B/A4 is the major component of brain amyloid plaque, one of the hallmarks of Alzheimer's disease (AD). 3 key findings →
Evidence: low
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Previous studies have shown a marked decline in neuronal and an increase in glial gene expression in Alzheimer's disease (AD) neocortex. 2 key findings →
Evidence: low
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Dementia arising in patients with Parkinson disease or parkinsonian neurodegeneration comprises a heterogeneous neuropathology. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Features of multipotentiality of engineered NSC-derived cell lines versus naive cells (control-NSC) were assessed by immunocytochemical analysis in differentiation conditions. 5 key findings →
Evidence: low
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Immunohistochemical staining with polyclonal antibodies to synthetic amyloid (residues 1-28 of A4) was performed on normal and Down syndrome brains from fetuses to adults. 1 key finding →
Evidence: low
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The present findings demonstrate several fundamental parallels between lens and neuron vesicle trafficking cell biology and development, and suggest that more extensive AbetaPP related vesicle trafficking disease mechanisms may be shared by lens and brain. 4 key findings →
Evidence: low
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Monoclonal antibodies (mAbs) D3G6 and C8A5, specific for amino acid residues 160-168 of S182 protein, immunolabeled neurons, ependymal and choroid plexus cells, and myocytes in brain sections from normal subjects and people with Alzheimer disease or Down syndrome and in rats and mice. 3 key findings →
Evidence: low
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Notch signaling is a master controller of the neural stem cell and neural development maintaining a significant role in the normal brain function. 1 key finding →
Evidence: low
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Down's syndrome (DS) is characterized by several pathological aspects leading to an increased susceptibility to cardiovascular diseases, infections, leukemia, endocrine alterations. 1 key finding →
Evidence: low
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In addition to the full-length beta-amyloid peptides (Aβ 1-40/42), several Aβ variants, truncated at their N- or C-termini and bearing different post-translational modifications, have been detected in the brain of Alzheimer´s disease (AD) patients. 2 key findings →
Evidence: low
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Tau protein promotes microtubule assembly. 1 key finding →
Evidence: low
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Down syndrome (DS) is one of the most common genetic diseases. 4 key findings →
Evidence: low
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It has been suggested that this increment, by accelerating hydrogen peroxide formation, might promote oxidative damage within DS cells and might be involved in the various neurobiological abnormalities found in DS such as premature aging and Alzheimer-type neurological lesions. 2 key findings →
Evidence: low
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Recently, an increasing number of genes have been associated with global developmental delay (GDD) and intellectual disability (ID). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Specifically, higher inflammation was associated with worse processing speed (B = -0.01; p < .05) and working memory (B = 8323.66; p < .1) only among those from more disadvantaged neighborhoods. 3 key findings →
Participants: 51 Evidence: low
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The onset and sustenance of Alzheimers and Parkinsons is solely dependent on the driving power of the immune cytokine interleukin-1 beta (IL-1β), arising from neuronal distress and release of sAPPα, which activates microglia for synthesis and release of IL-1β driving synthesis of βAPP, Aβ plaques and synthesis and activation of MAPKp38 for phosphorylation of tau for neurofibrillary tangle formation in Alzheimers and for a-synuclein for formation of Lewy bodies in Parkinsons. 1 key finding →
Evidence: low
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Alzheimer disease (AD) is a neurodegenerative disorder characterized by amyloid plaque deposition, neurofibrillary tangles, and chronic neuroinflammation. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Orally dosed D-AIP possessed favourable biostability, pharmacokinetics, and brain region distribution. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Like CP2, C458 and C273 weakly inhibit mtCI, leading to AMPK activation, which triggers a neuroprotective stress response. 5 key findings →
Evidence: low
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Vascular dementia (VaD) is recognized as the second most prevalent form of dementia after Alzheimer's disease, with its pathogenesis intricately associated with cerebrovascular pathologies, including chronic hypoperfusion, oxidative stress, and neuroinflammation. 2 key findings →
Design: narrative review Evidence: low
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MDVs are small vesicles that bud from mitochondria and play an important role in removing damaged mitochondrial components. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Microglia are central regulators of Alzheimer's disease pathogenesis, but their roles cannot be reduced to a simple protective-versus-harmful dichotomy. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
10 of the 8,313 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.
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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →