Protein misfolding is a fundamental biological process with profound implications for human health and disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Protein misfolding is a fundamental biological process with profound implications for human health and disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative disorders are devastating disorders characterized by gradual loss of neurons and cognition or mobility impairment. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Intraneuronal dysproteostasis and extraneuronal microenvironmental abnormalities in Alzheimer's disease (AD) collectively culminate in neuronal deterioration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by neuronal loss, cognitive decline, and pathological hallmarks such as amyloid-beta (Aβ) plaques and tau neurofibrillary tangles. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Evidence indicates that chronic proteotoxic stress, arising from aging, oxidative damage, and environmental influences, disrupts the proteostasis network (PN). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a complex neurodegenerative disease that affects elderly individuals, characterized by senile plaques formed by extracellular amyloid beta (Aβ). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Autophagy plays a pivotal role in the pathogenesis and progression of Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the primary cause of dementia in older individuals, exhibiting an increasing incidence worldwide. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia impact brain development, homeostasis, and pathology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Pathological tau disrupts protein homeostasis (proteostasis) within neurons in Alzheimer's disease (AD) and related disorders. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Chaperones are central to the proteostasis network (PN) and safeguard the proteome from misfolding, aggregation, and proteotoxicity. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mitochondrial dysfunction plays a preponderant role in the development of Alzheimer disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Most common clinical diagnosis was PSP (41%) for PSP; unspecified FTD (36%) for CBD; AD for AGD (57%) and Other-4R groups (48%), without sex differences. 5 key findings →
Participants: 175 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We identified several significant sex-specific and sex-dimorphic differentially expressed genes in neurons, microglia, astrocytes and oligodendrocytes, including both cross-sectional changes and alterations from 7 months to 17 months of age. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Emerging evidence suggests that viral infections may contribute to the onset and progression of Alzheimer's disease (AD) and other forms of dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A major hurdle in Alzheimer disease research is the failure of mouse models to capture complexities of the human brain that contributes to repeated clinical trial failure. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A wide range of human diseases are associated with protein misfolding and amyloid aggregates. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
It has been demonstrated to have neuroprotective effects in cellular models of neurodegenerative diseases; however, its precise mechanism of action in alleviating tau pathology in Alzheimer's disease (AD), as well as its potential to improve cognitive deficits in animal models, has not yet been elucidated. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Tri demonstrates significant multi-target neuroprotective effects in AD preclinical models. 2 key findings →
Design: systematic review Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The advanced glycation end-products (AGEs) are toxic molecules result from non-enzymatic interactions of sugar with lipids or proteins. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer’s disease (AD) is the leading cause of dementia in elderly individuals worldwide; however, all mechanisms leading to disease onset and progression are not well understood. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
All participants had heterozygous c.1184A > G, p.Asp395Gly in VCP. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The assembly of tau protein into amyloid filaments through templated seeding is believed to underlie the propagation of pathology in neurodegenerative diseases, such as Alzheimer's disease (AD) and other tauopathies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
• EEG microstate analyses were performed in a cohort of autosomal dominant AD. • Coverage of class C decreased in symptomatic mutation carriers • Coverage of class D decreased in presymptomatic and symptomatic mutation carriers. • Coverage of class E increased in presymptomatic and symptomatic mutation carriers. • The findings may support presymptomatic changes in resting-state neuronal networks. 4 key findings →
Participants: 99 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Amyloidoses, which are characterized by abnormal accumulation of amyloid proteins leading to organ dysfunction, represent a major therapeutic challenge. 2 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 27,380 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 →