Overall, symptoms in the last week and month of life did not vary by diagnosis. 4 key findings →
Participants: 286 Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
50/100
Absence of functional surrogate decision-makers is a major barrier to research and clinical decision-making for hospitalized patients with advanced dementia. 2 key findings →
Participants: 68 Evidence: high
Full summary, score breakdown and related studies → Original source
The preferences of end-of-life issues differed greatly between dementia patients and their caregivers. 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
The application of medical technology to prolong life at the expense of quality of life is widely debated in end-of-life care. 2 key findings →
Participants: 2,923 Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral cortical dysgenesis (CD) is a heterogeneous disorder of cortical development and organization commonly associated with epilepsy, with a variety of subtypes. 3 key findings →
Participants: 30 Evidence: low
Full summary, score breakdown and related studies → Original source
The adoption into the UK of children who have been reared in severely deprived conditions provides an opportunity to study possible association between very early negative experiences and subsequent brain development. 1 key finding →
Design: cross-sectional Participants: 14 Evidence: low
Full summary, score breakdown and related studies → Original source
We conclude that Aβ deposition is associated with a pattern of cortical thickness reduction consistent with AD prior to the development of cognitive impairment. 4 key findings →
Participants: 32 Evidence: low
Full summary, score breakdown and related studies → Original source
We recently demonstrated that the frequencies of biomarker groups defined by the presence or absence of both amyloidosis (A+) and neurodegeneration (N+) changed dramatically by age in cognitively non-impaired subjects. 4 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Reduced hippocampal volume has been reported in depression and may be involved in the aetiology of depressive symptoms and vulnerability to depressive relapse. 2 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Neuroimaging and postmortem studies of subjects with major depressive disorder (MDD) reveal smaller hippocampal volume with lengthening duration of illness. 4 key findings →
Design: cross-sectional Participants: 17 Evidence: low
Full summary, score breakdown and related studies → Original source
Both groups were compared with a sample of healthy control participants (n = 21). 5 key findings →
Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source
We hypothesized that cerebrospinal fluid (CSF) biomarkers of amyloid, neurodegeneration, and endothelial dysfunction would differ between older African Americans and Caucasians with normal cognition and cognitive impairment associated with AD. 3 key findings →
Participants: 135 Evidence: low
Full summary, score breakdown and related studies → Original source
50/100
We found that longitudinal measures of cortical atrophy were widely correlated with sleep quality. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cardiovascular risk factors, deregulated blood glucose, uric acid metabolism, and inflammation were identified as risk markers for faster disease progression. 2 key findings →
Participants: 135 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The purpose of this study is to explore the possibility of progressive neuropsychological decline in chronic temporal lobe epilepsy (TLE) and determine how this vulnerability may be associated with the neurodevelopmental impact of the disorder. 53 patients with TLE and 62 healthy controls underwent quantitative MRI volumetric imaging of total brain tissue and hippocampal volumes as well as assessment of intelligence and memory function. 5 key findings →
Design: cross-sectional Participants: 53 Evidence: low
Full summary, score breakdown and related studies → Original source
50/100
Relative to CN participants, Obj-SCD was associated with faster amyloid accumulation and selective vulnerability of entorhinal cortical thinning, whereas MCI was associated with faster entorhinal and hippocampal atrophy. 5 key findings →
Participants: 747 Evidence: low
Full summary, score breakdown and related studies → Original source
A significant association between childhood SES and hippocampal volumes in late life is consistent with the established neurodevelopmental findings that early life conditions have an effect on structural brain development. 2 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Intractable epilepsy is related to various transient and chronic brain electric and neurochemical disturbances. 3 key findings →
Design: cross-sectional Participants: 78 Evidence: low
Full summary, score breakdown and related studies → Original source
Broad clinical syndromes associated with COVID-19 were classified as a cerebrovascular event (defined as an acute ischaemic, haemorrhagic, or thrombotic vascular event involving the brain parenchyma or subarachnoid space), altered mental status (defined as an acute alteration in personality, behaviour, cognition, or consciousness), peripheral neurology (defined as involving nerve roots, peripheral nerves, neuromuscular junction, or muscle), or other (with free text boxes for those not meeting these syndromic presentations). 4 key findings →
Design: case report Participants: 153 Evidence: low
Full summary, score breakdown and related studies → Original source
Renal impairment is associated with an increased risk of carotid atherosclerosis and stroke, determinants of cognitive dysfunction and dementia. 5 key findings →
Participants: 3,349 Evidence: low
Full summary, score breakdown and related studies → Original source
50/100
The results suggest that the hippocampus and the temporal horn of the lateral ventricles may be useful as antemortem markers of AD in mildly impaired patients. 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
These data weakly corroborate prior findings of associations between LTL and mortality in the elderly. 3 key findings →
Participants: 1,136 Evidence: low
Full summary, score breakdown and related studies → Original source
Our data suggest that a single explanation for poststroke dementia is not adequate; rather, multiple factors including stroke features (dysphasia, major dominant stroke syndrome), host characteristics (educational level), and prior cerebrovascular disease each independently contribute to the risk. 3 key findings →
Participants: 30 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our findings confirm previous research on the specific roles of CA1 and subiculum in episodic memory. 4 key findings →
Participants: 133 Evidence: low
Full summary, score breakdown and related studies → Original source
CSF biomarkers and amyloid positron emission tomography reflect different aspects of Alzheimer's disease brain pathology, and therefore, less-than-perfect correspondence is expected. 1 key finding →
Participants: 200 Evidence: low
Full summary, score breakdown and related studies → Original source
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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 28,180 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.
What this library is — and isn't
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →