27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The memory-enhancing effect of IVIg reported here suggests that Aβ oligomers, effector T cells and the fractalkine pathway are potential pharmacological targets of IVIg in AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is the public health crisis of the 21st century. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common and devastating dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Compared with ERP, MRI, or neuropsychological tests alone, the VR-DOT could provide additional predictive information in a low-cost, computerized, and noninvasive way. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The immune response, regulation of endocytosis, cholesterol transport, and protein ubiquitination represent prime targets for AD therapeutics. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Experimental studies of Alzheimer's disease have largely depended on transgenic mice overexpressing amyloid precursor protein (APP). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The goal of this review is to discuss how behavioral tests in mice relate to the pathological and neuropsychological features seen in human Alzheimer's disease (AD), and present a comprehensive analysis of the temporal progression of behavioral impairments in commonly used AD mouse models that contain mutations in amyloid precursor protein (APP). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Astrocytic network alterations have been reported in Alzheimer's disease (AD), but the underlying pathways have remained undefined. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microtubule-associated protein tau encoded by the MAPT gene binds to microtubules and is important for maintaining neuronal morphology and function. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The aim of this study was to determine whether the TAR DNA-binding protein of 43 kDa (TDP-43) has any independent effect on the clinical and neuroimaging features typically ascribed to Alzheimer's disease (AD) pathology, and whether TDP-43 pathology could help shed light on the phenomenon of resilient cognition in AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
For the last decade, it has been shown that neuroimaging can be a potential tool for the diagnosis of Alzheimer's Disease (AD) and its prodromal stage, Mild Cognitive Impairment (MCI), and also fusion of different modalities can further provide the complementary information to enhance diagnostic accuracy. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Nutraceuticals are products, which other than nutrition are also used as medicine. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tauroursodeoxycholic acid (TUDCA) is the taurine conjugate of ursodeoxycholic acid (UDCA), a US Food and Drug Administration-approved hydrophilic bile acid for the treatment of certain cholestatic liver diseases. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The amyloid cascade hypothesis has been the prevailing hypothesis in Alzheimer's Disease research, although the final and most wanted proof i.e. fully successful anti-amyloid clinical trials in patients, is still lacking. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Proteinaceous inclusions are common hallmarks of many neurodegenerative diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Inhibitions of amyloid β (Aβ) aggregation and Aβ-haem peroxidase-like activity have received much attention because these two symptoms can be the primary targets of therapeutic strategies for Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The symptomatic drugs currently on the market for Alzheimer's disease (AD) have no effect on disease progression, and this creates a large unmet medical need. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Protein misfolding and aggregation are associated with more than twenty diseases, such as neurodegenerative diseases and metabolic diseases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Current treatment options for Alzheimer's disease (AD) are limited to medications that reduce dementia symptoms. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aβ immunotherapy for Alzheimer's disease (AD) results in the removal of Aβ plaques and increased cerebral amyloid angiopathy (CAA). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The severity of tau pathology in Alzheimer's disease brain correlates closely with disease progression. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aggregates of hyperphosphorylated tau protein are found in a group of diseases called tauopathies, which includes Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We have discovered defined determinants on mis-disordered truncated tau protein which are responsible for tau oligomerisation leading to neurofibrillary degeneration. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Perhaps more definitively than any other class of novel Alzheimer's disease (AD) therapy, pre-clinical studies in mouse models of amyloid β (Aβ) deposition have established the disease-modifying potential of anti-Aβ immunotherapy. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common cause of dementia and a major contributor to disability and dependency among older people. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →