28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Changes in the metabolic activity within the brain of patients suffering from Alzheimer's disease (AD) were investigated and compared with biochemical alterations in the hippocampus induced by fimbria/fornix transection in the rat. 5 key findings →
Evidence: low
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Alzheimer type II astrocytosis is the pathological hallmark of hepatic encephalopathy. 3 key findings →
Evidence: low
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This study offers evidence of functional and neuroprotective effects of two weeks treatment with a Ptychopetalum olacoides extract against Aβ peptide-induced neurotoxicity in mice. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Transmissible encephalopathies (TSEs), such as Creutzfeldt-Jakob disease (CJD) and scrapie, are caused by infectious agents that provoke strain-specific patterns of disease. 2 key findings →
Evidence: low
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Frontotemporal dementia regards a group of presenile progressive neurodegenerative form of dementias which includes Pick's disease, corticobasal degeneration, frontotemporal dementia with motor neuron disease, frontal lobe degeneration, dementia-parkinsonism-amyotrophy complex, familial non-specific dementia mapping to chromosome 3, non-Alzheimer degenerative dementia lacking distinctive histological features as well as a number other infrequent syndromes with dementia and focal neurological signs. 1 key finding →
Evidence: low
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A Doença de Alzheimer (DA) é a principal causa de demência no mundo, caracterizada por processos neurodegenerativos progressivos que comprometem cognição, comportamento e funcionalidade. 5 key findings →
Evidence: low
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Women have twice the dementia risk compared with men. 1 key finding →
Evidence: low
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Theranostics—the use of diagnostic and therapeutic drugs that target the same molecular marker of disease—extends beyond the paradigm of radiopharmaceutical drug pairs used in oncologic settings (e.g., somatostatin receptor subtype 2 and prostate-specific membrane antigen theranostics) to other 1 key finding →
Evidence: low
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A neuropathological study of Alzheimer type I (Alz I) and Alzheimer type II (Alz II) as well as Opalski (Opl) cells was performed serially on brain tissue from nine autopsied Wilson's disease (WD) cases. 5 key findings →
Evidence: low
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This study compared the relationships of the development of both Alzheimer I & II cells to reactive astrogliosis and also their distributional patterns in the demyelinated and non-demyelinated lesions in 6 cases of Wilson's disease by the use of PAP immunohistochemical technique for glial fibrillary acidic protein (GFAP). 5 key findings →
Evidence: low
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A study on long-term astrocytic responses (from 1 day to 20 months after lesioning in 4-month-old rats, and from 1 day to 6 months in 20-month-old rats) to diverse unilateral damage of the nucleus basalis (nbM) by injection of 40 nmol of ibotenic acid, or 50 or 100 nmols of quisqualic acid was performed using a histochemical method (immunoreactivity against the glial fibrillary acidic protein GFAP). 5 key findings →
Evidence: low
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[3H]inositol(1,4,5)-trisphosphate (IP3) binding studies have shown decreased [3H]IP3 binding to brain tissue in several neurodegenerative diseases, including Alzheimer's and Huntington's diseases. 2 key findings →
Evidence: low
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Anemia and iron deficiency are common in older adults, yet their relevance to blood biomarkers for Alzheimer disease (AD) remains underappreciated. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The deep-learning network was capable of learning the task of delineating pathologic and normal findings within minutes on a standard PC and performing the classification task with 100% accuracy in less than 1 millisecond per case. 5 key findings →
Participants: 20 Evidence: low
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12.05.2026: Debatt - En enkel blodprøve kan nå påvise fosforylert tau-protein 217 (p-tau217) – et biologisk tegn på Alzheimers sykdom, som kan være til stede mange år før de første symptomene viser seg. 1 key finding →
Evidence: low
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In Transmissible Spongiform Encephalopathies (TSEs) and Alzheimer disease (AD) both misfolding and aggregation of specific proteins represent key features. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A 77-year-old woman with mild cognitive impairment was referred to 18F-florbetapir positron emission tomography (PET) to assess the indication of a disease-modifying drug against Alzheimer disease. 5 key findings →
Evidence: low
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Alzheimer Disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-β deposition, tau pathology, synaptic dysfunction, neuronal injury and cerebral atrophy. 1 key finding →
Evidence: low
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In human brain extracts, most proteins of pathological interest in Alzheimer's disease are insoluble and their analysis is often performed on denatured and reduced samples by immunoblotting after electrophoresis on polyacrylamide gel in presence of sodium dodecyl sulfate. 3 key findings →
Evidence: low
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The most successful amyloid-targeting treatments achieve modest plaque reduction with marginal clinical benefit and significant adverse effects. 1 key finding →
Evidence: low
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The dominant research paradigm for Alzheimer's disease has focused on amyloid-beta plaqueremoval for over three decades, producing no curative therapy despite billions of dollars ofinvestment. 2 key findings →
Evidence: low
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Manganese-superoxide dismutase (Mn-SOD) was localized in the cerebral cortex and hippocampus of patients with Alzheimer-type senile dementia (ATD) by immunocytochemistry and the relationship of Mn-SOD with two major pathological features of ATD, i.e., senile plaques and neurofibrillar tangles (NFTs), was examined. 2 key findings →
Evidence: low
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Early hypoxic-ischemic brain lesions were examined regarding 26 autopsy cases which had severe asphyxia at birth and died within the first week. 1 key finding →
Evidence: low
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The research focuses on the use of biomarkers to diagnose Alzheimer’s disease (AD) in living individuals. 5 key findings →
Evidence: low
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Eine von 5 Frauen und einer von 10 Männern entwickeln eine Demenz vom Alzheimer-Typ, erläutern Palmqvist et al. zu Beginn ihrer Studie [1]. 5 key findings →
Evidence: low
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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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →