30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
The pattern of degenerative changes in the brain white matter (WM) in aging, mild cognitive impairment (MCI), and Alzheimer's disease (AD) has been under debate. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) has a slow onset, so it is challenging to distinguish brain changes in healthy elderly persons from incipient AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Structural brain changes have been described in both mild cognitive impairment (MCI) and Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Effectively, modern research has confirmed Hortega's view of the origin of the microgliacyte from circulating monocytes of the monocyte-macrophage series that invade the brain during embryonic and early postnatal life. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
MSE measures identified an abnormal complexity profile across different temporal scales and their relation to the severity of AD. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Resting-state functional magnetic resonance imaging (fMRI), a promising technique for measuring brain activities during rest, has attracted much attention in the past few years. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by cognitive decline and neuronal network dysfunction, but the underlying mechanisms remain unknown. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In recent years there has been increased interest in whether vascular disease contributes to Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A quantitative and clincally correlated investigation was carried out to determine the divisional distribution of volumetric and cell-packing density changes in the amygdala in patients with advanced aging and senile dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cognitive dysfunction can occur in some patients with amyotrophic lateral sclerosis (ALS) who are not suffering from dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral volume loss has long been associated with normal aging, but whether this is due to aging itself or to age-related diseases, including incipient Alzheimer disease, is uncertain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study aimed to investigate the atrophy of the posterior cingulate cortex (PCC) and medical temporal lobe (MTL) structures (i.e., the entorhinal cortex (ERC) and hippocampus) and the regional disruption of the cingulum bundle in mild cognitive impairment (MCI) and Alzheimer's disease (AD) patients. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Polygenetic risk factors and reduced expression of many genes in late-onset Alzheimer's disease (AD) impedes identification of a target(s) for disease-modifying therapies. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Much of the research on delaying the onset of symptoms of Alzheimer's disease (AD) has focused on pharmacotherapy, but environmental factors have also been acknowledged to play a significant role. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amnestic type mild cognitive impairment (aMCI) refers to a transitional stage between normal aging and Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer disease (AD) is pathologically characterized by cortical atrophy. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Effects of normal aging such as loss of PCC co-activity could be detected by ICA, but not by signal time course correlation analyses of DMN inter-connectivity. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We found evidence for functionally relevant microstructural changes in the NAWM of patients with AD and MCI. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In contrast to the tremendous amount of research data from the central nervous system, relatively little is known about microglial homeostasis in the retina. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal dementia (FTD) and Huntington's disease (HD) are degenerative disorders, with predominant involvement, respectively of frontal neocortex and striatum. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The frontal cortex, generally vulnerable in Alzheimer's disease, had higher concentrations of all analytes than the occipital cortex which is generally unaffected. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The extensive networking of the cells of the nervous system results in large cell membrane surface areas. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a common, incurable, and progressive dementia, characterized by loss of learning and memory and the neuropathologic accumulation of amyloid plaques and neurofibrillary tangles in the brain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Heat shock proteins (Hsps) are highly conserved and under physiological conditions act as molecular chaperones and/or have anti-apoptotic activities. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the homozygous and heterozygous states, GBA mutations are associated with a spectrum of parkinsonian phenotypes ranging from Parkinson disease, mostly of the akinetic type, to a less common phenotype characteristic of Lewy body dementia. 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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events