Wakefulness, along with fast cortical rhythms and associated cognition, depend on the basal forebrain (BF). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Research increasingly suggests that subjective cognitive decline (SCD) in older adults, in the absence of objective cognitive dysfunction or depression, may be a harbinger of non-normative cognitive decline and eventual progression to dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
52/100
Maintaining DNA integrity is vital for all cells and organisms. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Common single nucleotide polymorphisms in the SORL1 gene have been associated with late onset Alzheimer disease (LOAD), but causal variants have not been fully characterized nor has the mechanism been established. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Clearing cellular debris after brain injury represents an important mechanism in regaining tissue homeostasis and promoting functional recovery. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Data sources EMBASE, CINAHL, MEDLINE, PsychInfo. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This is the first study to assess cerebral microinfarcts (CMIs) on 3 tesla (3T) magnetic resonance imaging (MRI) in a memory clinic population. 4 key findings →
Participants: 238 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
52/100
Additionally, we investigated the relation between cardiac function and MRI markers of subclinical cerebrovascular disease. 4 key findings →
Participants: 3,291 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Given the recent acknowledgement of the complex mixed pathologies that contribute to the clinical expression of dementia, various cohort studies have aimed to examine Alzheimer's disease and cerebrovascular disease as comorbid pathologies, with neuroimaging playing a central role in these studies. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
52/100
We studied the biomarker signatures and prognoses of 3 different subtle cognitive impairment (SCI) groups (executive, memory, and multidomain) as well as the subjective memory complaints (SMC) group. 4 key findings →
Participants: 522 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Disturbances in the sleep-wake cycle and circadian rhythms are common symptoms of Alzheimer Disease (AD), and they have generally been considered as late consequences of the neurodegenerative processes. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Reported rates of dementia differ by race, although most studies have not focused on carefully measured outcomes, confounding by education or other demographic factors, nor have they studied other outcomes other than dementia. 1 key finding →
Participants: 15,792 Evidence: moderate
Full summary, score breakdown and related studies → Original source
52/100
Scores on the full and abbreviated versions of the MoCA can be linked directly to the MMSE. 1 key finding →
Design: cross-sectional Participants: 199 Evidence: low
Full summary, score breakdown and related studies → Original source
Overall, patients dying as a result of non-cancer diseases were twice as likely to be admitted to ICUs at the EOL as patients dying due to cancer. 5 key findings →
Participants: 240,757 Evidence: low
Full summary, score breakdown and related studies → Original source
These cross-sectional results suggest that cortical changes (regional-specific damage and network breakdown), mediated (in)directly by WMH (tract-specific damage) and other factors (eg, vascular risk factors), might lead to cognitive decline. 5 key findings →
Design: cross-sectional Participants: 426 Evidence: low
Full summary, score breakdown and related studies → Original source
In patients with a discrepancy between CSF p-tau181 and CSF Aβ42, the assessment of Aβ 42/40 ratio led to a reliable biological conclusion in over 50% of cases that agreed with a clinician's diagnosis. 1 key finding →
Participants: 367 Evidence: low
Full summary, score breakdown and related studies → Original source
The two main findings of this paper are (i) the posterior default mode network fails before measurable amyloid plaques and appears to initiate a connectivity cascade that continues throughout the disease spectrum; and (ii) high connectivity between the posterior default mode network and hubs of high connectivity (many located in the frontal lobe) is associated with amyloid accumulation. 2 key findings →
Participants: 128 Evidence: low
Full summary, score breakdown and related studies → Original source
Type 2 diabetes mellitus and Alzheimer's disease are both associated with increasing age, and each increases the risk of development of the other. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Specific neuropsychiatric symptoms are associated with shorter survival time from mild Alzheimer's dementia to severe dementia and/or death. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Utilization patterns of psychotropic drugs in institutionalized patients with dementia have changed over the past decade. 4 key findings →
Participants: 49,251 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma DES/CHO was significantly reduced in Japanese AD patients and significantly correlated with Mini-Mental State Examination (MMSE) score. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
In HC and MCI subjects, FBP PET anterior and posterior cingulate and composite standard uptake value ratios correlated with CSF amyloid beta (Aβ1-42) and tau/Aβ1-42 ratios. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cerebral microbleeds (CMBs) are hypothesised to have an important yet unknown role in the dementia disease pathology. 4 key findings →
Participants: 1,039 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The study results identified that dementia-related factors were the most significant factors, representing 25.6% of caregiver burden and were followed by caregiving-related factors explaining caregiver burden significantly. 3 key findings →
Participants: 1,133 Evidence: low
Full summary, score breakdown and related studies → Original source
RVT-101 is a 5-hydroxytryptamine 6 (5-HT6) receptor antagonist for the treatment of dementia with a number of favorable properties including once daily dosing, lack of food effect, and low potential for drug interactions. 4 key findings →
Design: clinical trial Participants: 684 Evidence: high
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.
1,034 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 →