27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Reduction of brain amyloid-β (Aβ) has been proposed as a therapeutic target for Alzheimer disease (AD), and microglial Aβ phagocytosis is noted as an Aβ clearance system in brains. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Diabetes and Alzheimer disease (AD)-two age-related diseases-are both increasing in prevalence, and numerous studies have demonstrated that patients with diabetes have an increased risk of developing AD compared with healthy individuals. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Several neurodegenerative diseases are typified by intraneuronal alpha-synuclein deposits, synaptic dysfunction, and dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer disease (AD) is the most common neurodegenerative disorder worldwide and is at present, incurable. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Despite the progress of the past two decades, the cause of Alzheimer's disease (AD) and effective treatments against it remain elusive. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) and ageing are associated with impaired learning and memory, and recent findings point toward modulating chromatin remodeling through histone acetylation as a promising therapeutic strategy. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Parkinson's disease (PD), a progressive neurodegenerative disease, results in abnormal accumulation of insoluble alpha-synuclein (alpha-Syn) in dopaminergic neurons. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Reduced clearance of amyloid β peptides (Aβ) across the blood-brain barrier contributes to amyloid accumulation in Alzheimer disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dephosphorylation (activation) of cofilin, an actin binding protein, is stimulated by initiators of neuronal dysfunction and degeneration including oxidative stress, excitotoxic glutamate, ischemia, and soluble forms of beta-amyloid peptide (Abeta). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Synaptic transmission is essential for nervous system function, and its dysfunction is a known major contributing factor to Alzheimer's-type dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although the pathogenesis of sporadic Alzheimer disease (AD) is not clearly understood, it is likely dependent on several age-related factors. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The receptor for advanced glycation end products (RAGE) is a pattern-recognition receptor that binds to diverse ligands and initiates a downstream proinflammatory signaling cascade. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau protein in a hyperphosphorylated state makes up the intracellular inclusions of several neurodegenerative diseases, including Alzheimer's disease and cases of frontotemporal dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Soluble oligomeric aggregates of the amyloid-beta (A beta) peptide are believed to be the most neurotoxic A beta species affecting the brain in Alzheimer disease (AD), a terminal neurodegenerative disorder involving severe cognitive decline underscored by initial synaptic dysfunction and later extensive neuronal death in the CNS. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The risk for dementia, a major contributor to incapacitation and institutionalization, rises rapidly as we age, doubling every 5 y after age 65. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurofibrillary tangles (NFTs), which consist of highly phosphorylated tau, are hallmarks of neurodegenerative diseases including Alzheimer disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aging is the most important single risk factor for developing Alzheimer disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The blood-brain barrier (BBB) not only impedes the influx of intravascular substances from blood to brain, but also promotes transport of substances from blood to brain or from brain to blood through several transport systems such as carrier-mediated transport, active efflux transport, and receptor-mediated transport systems. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
CT offers promise as a preventive therapeutic technique in healthy older adults and particularly as a secondary prevention method for "at risk" groups. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Converging lines of research indicate that complex mental activity is associated with reduced dementia risk. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
As the population ages, risks for cognitive decline threaten independence and quality of life for older adults and present challenges to the health care system. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Regular physical activity undoubtedly has many health benefits for all age groups. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
As the number of patients with Alzheimer's disease (AD) is expected to grow, finding ways to prevent and lower the risk of AD becomes a crucial matter. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Severe nutritional deficiencies, such as protein energy malnutrition and deficiency of nicotinamide, vitamin B(12), folate, and thiamine, have long been recognized to cause severe confusion. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Delirium and dementia share similarities in clinical and pathogenic features, leading to the speculation that instead of being distinct clinical entities, the two age-related conditions may be linked by a common pathogenic mechanism. 5 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 →