The concept of molecular mimicry was established to explain commonalities of structure which developed in response to evolutionary pressures. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
29,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The concept of molecular mimicry was established to explain commonalities of structure which developed in response to evolutionary pressures. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
DNA methylation is a major epigenetic modification that regulates gene expression. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
By comparing the cerebrospinal fluid (CSF) proteome between Alzheimer's disease (AD) patients and controls, it may be possible to identify proteins that play a role in the disease process and thus to study the pathogenesis of AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
An increasing body of evidence indicates that oxidative stress and damage play a role in the pathogenesis of a number of diseases associated with neurodegeneration, including Down syndrome (DS), Alzheimer's disease (AD) and Pick's disease (PD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Defects in lysosomal function have been associated with numerous monogenic human diseases typically classified as lysosomal storage diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Epigenetic modifications represent mechanisms by which cells may effectively translate multiple signaling inputs into phenotypic outputs. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microtubule-associated Tau proteins belong to a family of factors that polymerize tubulin dimers and stabilize microtubules. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A PET tracer is desired to help guide the discovery and development of disease-modifying therapeutics for neurodegenerative diseases characterized by neurofibrillary tangles (NFTs), the predominant tau pathology in Alzheimer disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We found that Tau and amyloid-β deposits are associated with distinctive spatial patterns of brain tissue loss. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurofibrillary tangles (NFTs) made up of aggregated tau protein have been identified as the pathologic hallmark of several neurodegenerative diseases including Alzheimer's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Accumulating evidence suggests that subjective cognitive complaints (SCC) may indicate subtle cognitive decline characteristic of individuals with preclinical Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Gray matter atrophy, glucose hypometabolism, and β-amyloid Aβ deposition are well-described hallmarks of Alzheimer's disease, but their relationships are poorly understood. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The amyloid cascade hypothesis suggests that the aggregation and deposition of amyloid-beta protein is an initiating event in Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although beta-amyloid (Aβ) deposition is a characteristic feature of Alzheimer's disease (AD), this pathology is commonly found in elderly normal controls (NC). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
During the development of in vivo amyloid imaging agents, an effort was made to use micro-positron emission tomography (PET) imaging in the presenilin-1 (PS1)/amyloid precursor protein (APP) transgenic mouse model of CNS amyloid deposition to screen new compounds and further study Pittsburgh Compound-B (PIB), a PET tracer that has been shown to be retained well in amyloid-containing areas of Alzheimer's disease (AD) brain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Midlife may be an ideal window for intervention in Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
(18)F-labeled THK-5105 and THK-5117 are promising candidates as PET tau imaging radiotracers. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This paper introduces neurite orientation dispersion and density imaging (NODDI), a practical diffusion MRI technique for estimating the microstructural complexity of dendrites and axons in vivo on clinical MRI scanners. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our brain is a network. It consists of spatially distributed, but functionally linked regions that continuously share information with each other. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Quantification of non-Gaussianity for water diffusion in brain by means of diffusional kurtosis imaging (DKI) is reviewed. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The function of neural circuits and networks can be controlled, in part, by modulating the synchrony of their components' activities. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This review considers recent advances in the application of resting-state functional magnetic resonance imaging to the study of neuropsychiatric disorders. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent research on Alzheimer's disease (AD) has shown that cognitive and memory decline in this disease is accompanied by disrupted changes in the coordination of large-scale brain functional networks. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Many complex and interesting phenomena in nature are due to nonlinear phenomena. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
It is commonly assumed that functional brain connectivity reflects structural brain connectivity. 1 key finding →
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 29,380 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 29,380 records, built mostly from automated pulls of Europe PMC (63.3% of the library) and OpenAlex (17.3%), 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.
1,037 records (3.5% of the library) are not peer-reviewed — 964 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 →