27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Our findings suggest that restoration of the expression of nuclear-encoded OXPHOS genes in aging could be a viable strategy for blunting AD progression. 4 key findings →
Evidence: low
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Mild cognitive impairment (MCI) represents a transitional stage between normal aging and dementia, often considered critical for dementia prevention. 1 key finding →
Evidence: low
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At baseline, SCDp were older, had a higher prevalence of hypertension and hypercholesterolemia and had worst performance on tests related to processing speed, verbal fluency, visual memory, verbal memory, and executive functioning. 4 key findings →
Participants: 450 Evidence: low
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Alzheimer's disease (AD) is a complex, progressive, and irreversible neurodegenerative disorder marked by cognitive decline and memory loss. 1 key finding →
Evidence: low
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Mild cognitive impairment (MCI) is a condition characterized by noticeable deficits in memory retrieval or other cognitive domains than the individuals with the same age but do not significantly interfere with daily functioning. 2 key findings →
Design: longitudinal study Evidence: moderate
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The aim of this study is to build and validate a model based on structural magnetic resonance imaging (sMRI) to predict the progression of mild cognitive impairment (MCI) to Alzheimer's disease (AD). 3 key findings →
Participants: 240 Evidence: low
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Amyloid‐reactive T cell polyfunctional response distinguishes MCI from normal aging and could serve as a novel MCI biomarker. 4 key findings →
Evidence: moderate
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Our results indicate that decline in semantic fluency is an early indicator of cognitive deficits in preclinical Alzheimer's disease. 5 key findings →
Participants: 490 Evidence: low
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A total of 1,223 articles were identified. 5 key findings →
Participants: 1,223 Evidence: low
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In amnestic mild cognitive impairment (aMCI), neuroinflammation evolves during disease progression, affecting microglial function and potentially accelerating the pathological process. 4 key findings →
Evidence: high
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Event-related potentials (ERPs), particularly the P200 component, have been studied as potential biomarkers, but conventional grand-averaged approaches often yield inconsistent results. 5 key findings →
Participants: 636 Evidence: moderate
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Multicomponent and transdisciplinary interventions focused on the family member–patient dyad have the potential to optimize cognitive outcomes and quality of life. 1 key finding →
Participants: 40 Evidence: high
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Individuals experiencing complications, such as worsening symptoms and functional impairment when a medication dose wears off ("off periods"), medication-resistant tremor, and dyskinesias, benefit from advanced treatments such as therapy with levodopa-carbidopa enteral suspension or deep brain stimulation. 5 key findings →
Evidence: low
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Memory function is likely subserved by multiple distributed neural networks, which are disrupted by the pathophysiological process of Alzheimer's disease (AD). 5 key findings →
Participants: 52 Evidence: low
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In order to assess peripheral levels and activities of a broad spectrum of non-enzymatic and enzymatic antioxidants in elderly subjects with mild cognitive impairment (MCI) and Alzheimer's disease (AD), plasma levels of water-soluble (Vitamin C and uric acid) and of lipophilic (Vitamin A, Vitamin E and carotenoids including lutein, zeaxanthin, beta-cryptoxanthin, lycopene, alpha- and beta-carotene) antioxidant micronutrients as well as activities of plasma and red blood cell (RBC) superoxide dismutase (SOD) and of plasma glutathione peroxidase (GPx) were measured in 25 patients with MCI, 63 AD patients and 53 controls. 1 key finding →
Participants: 25 Evidence: low
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Alzheimer's disease (AD) is a highly disabling progressive neurodegenerative disorder characterized by a steadily growing number of patients, by the absence of a cure for the disease and by great difficulties in diagnosing in the preclinical phase. 1 key finding →
Evidence: low
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The field of aging and dementia research is advancing rapidly toward the stage of earlier identification of clinical symptoms. 5 key findings →
Evidence: low
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Enolase enzymes are abundantly expressed, cytosolic carbon-oxygen lyases known for their role in glucose metabolism. 3 key findings →
Evidence: low
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These data provide potential insights into the biology of CSF in AD and MCI progression and provide a novel tool for AD researchers and clinicians working to improve diagnostic accuracy, evaluation of treatment efficacy, and early diagnosis. 3 key findings →
Evidence: low
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Parkinson's disease (PD) is the second most common progressive neurodegenerative disorder mainly in middle-elderly population, which represents diverse nonmotor symptoms (NMS) besides such well-documented motor symptoms as bradykinesia, resting tremor, rigidity, and postural instability. 1 key finding →
Evidence: low
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The amnestic mild cognitive impairment/non-amnestic mild cognitive impairment separation is not only theoretical but backed by structural imaging methods and neuropsychological tests. 4 key findings →
Evidence: low
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Proteolytic processing and phosphorylation of amyloid precursor protein (APP), and hyperphosphorylation of tau protein, have been shown to be increased in Alzheimer's disease (AD) brains, leading to increased production of beta-amyloid (Abeta) peptides and neurofibrillary tangles, respectively. 2 key findings →
Evidence: low
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All cells rely on efficient protein synthesis in order to maintain cellular homeostasis. 2 key findings →
Evidence: low
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A possible role of vascular and lifestyle-related factors was recently proposed for age-related changes of cognitive function, predementia syndromes, and cognitive decline of degenerative (Alzheimer's disease, AD) or vascular origin (vascular dementia, VaD). 4 key findings →
Evidence: low
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Several recent studies indicate that activity of cholinergic enzymes in the cortex of people with mild cognitive impairment (MCI) and early Alzheimer's disease (AD) are preserved. 3 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 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 →