During the course of normal aging, biological changes occur in the brain that are associated with changes in cognitive ability. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
During the course of normal aging, biological changes occur in the brain that are associated with changes in cognitive ability. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A recently identified variant within the fat mass and obesity-associated (FTO) gene is carried by 46% of Western Europeans and is associated with an approximately 1.2 kg higher weight, on average, in adults and an approximately 1 cm greater waist circumference. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Rapid advances in neuroimaging techniques provide great potentials for study of Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Chronic neuroinflammation correlates with cognitive decline and brain atrophy in Alzheimer's disease (AD), and cytokines and chemokines mediate the inflammatory response. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our results suggest that the COSLOF index could be used as a noninvasive quantitative marker for the preclinical stage of AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Increasing the lifespan of a population is often a marker of a country's success. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The perforant path (PP) undergoes synaptic changes in the course of aging and dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We illustrate these methods principally by showing that there are significant differences between patients with early Alzheimer's disease (AD) and age-matched comparison subjects in the persistence of fGn in the medial and lateral temporal lobes, insula, dorsal cingulate/medial premotor cortex, and left pre- and postcentral gyrus: patients with AD had greater persistence of resting fMRI noise (larger H) in these regions. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Over the next 20 years the number of Americans diagnosed with dementia is expected to more than double (CDC, 2007). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Graph theoretical analysis of structural and functional connectivity MRI data (ie. diffusion tractography or cortical volume correlation and resting-state or task-related (effective) fMRI, respectively) has provided new measures of human brain organization in vivo. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
WMH may represent foci of more widespread and subtle white matter changes rather than distinct, sharply delineated anatomic abnormalities. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Resting-state networks dissociate in the early stage of Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
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 →