27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease (AD) is an irreversible brain disorder characterized by progressive cognitive decline and neurodegeneration of brain regions that are crucial for learning and memory. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In mature neurons, the number of synapses is determined by a neuronal activity-dependent dynamic equilibrium between positive and negative regulatory factors. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementias are a varied group of disorders typically associated with memory loss, impaired judgment and/or language and by symptoms affecting other cognitive and social abilities to a degree that interferes with daily functioning. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
One of the shared hallmarks of neurodegenerative diseases is the accumulation of misfolded proteins. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Impairment of the ubiquitin-proteasome system (UPS) has been implicated in the pathogenesis of a wide variety of neurodegenerative disorders, including Alzheimer's, Parkinson's, and Huntington's diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cellular proteomes are continuously undergoing alterations as a result of new production of proteins, protein folding, and degradation of proteins. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The research on aging and age-related diseases, especially the neurodegenerative diseases, is on the fast track. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Proteostasis are integrated biological pathways within cells that control synthesis, folding, trafficking and degradation of proteins. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Impaired protein degradation has been discussed as a cause or consequence of various neurodegenerative diseases, such as Alzheimer's, Parkinson's and Huntington's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cells have developed an evolutionary obligation to survey and maintain proteome fidelity and avoid the possible toxic consequences of protein misfolding and aggregation. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The extracellular aggregation of proteins into proteotoxic oligomers and amyloid fibrils is implicated in the onset and pathology of numerous diseases referred to as amyloid diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The autophagic process is the only known mechanism for mitochondrial turnover and it has been speculated that dysfunction of autophagy may result in mitochondrial error and cellular stress. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glyphosate, the active ingredient in Roundup®, is the most popular herbicide used worldwide. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tauopathies, including Alzheimer's disease (AD) and Frontotemporal Dementia (FTD), are histopathologically defined by the aggregation of hyperphosphorylated pathological tau (pTau) as neurofibrillary tangles in the brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
GRc exerted neuroprotective effects in VaD by targeting Stat3 and driving its dual-phosphorylation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Tauopathies are neurodegenerative diseases characterized by accumulation of hyperphosphorylated tau protein (P-tau). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In plasma, most complement analytes were not significantly different between spFTD and HC; the exceptions were C4 and FB, significantly decreased in spFTD vs HC ( p = 0.0192 and p = 0.0181, respectively), suggesting complement consumption in classical and alternative pathways. 3 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In the AD continuum group, all cognitive test performances significantly correlated with tracer uptake, particularly in the left cortical areas. 4 key findings →
Participants: 120 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's Disease (AD) is the most common dementia, affecting mainly older adults, particularly over 65. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The amyloid hypothesis is the predominant model of Alzheimer's disease (AD) pathogenesis, suggesting that amyloid beta (Aβ) peptide is the primary driver of neurotoxicity and a cascade of pathological events in the central nervous system. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In this study, the rank of multifaceted activity of catechin (C), epicatechin (EC), epigallocatechin (EGC), epicatechin-3-gallate (ECG) and epigallocatechin-3-gallate (EGCG) was addressed. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD), a leading cause of dementia worldwide, is a multifactorial neurodegenerative disorder characterized by amyloid-beta plaques, tauopathy, neuronal loss, neuro-inflammation, brain atrophy, and cognitive deficits. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Misfolding and aggregation of microtubule-associated tau protein is implicated in a variety of neurodegenerative disorders (named tauopathies), including Alzheimer's disease (AD) and chronic traumatic encephalopathy (CTE). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Tauopathies, including Alzheimer's disease and frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17), are characterized by the aberrant aggregation of tau protein into neurofibrillary tangles. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the most prevalent cause of dementia and can be conceptualized as a tauopathy initiated by the accumulation of amyloid-β (Aβ) in the brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 →