30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Limbic-predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) and Alzheimer's disease neuropathologic change (ADNC) are each associated with substantial cognitive impairment in aging populations. 2 key findings →
Design: longitudinal study Participants: 5,665 Evidence: moderate
Full summary, score breakdown and related studies → Original source
SNAP-25 and 14-3-3 zeta/delta also had the strongest associations with tau-PET, amyloid-β-PET and cortical thickness at baseline and were associated with longitudinal changes in these imaging biomarkers [β(standard error, SE) = -0.056(0.0006) to 0.058(0.005), P < 0.0001]. 3 key findings →
Design: longitudinal study Participants: 205 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This population-based cohort study demonstrates significant association between IBD and subsequent development of dementia. 5 key findings →
Design: cohort study Participants: 1,742 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Serum IgG levels to common periodontal microbiota are associated with risk for developing incident AD. 5 key findings →
Design: cohort study Participants: 219 Evidence: moderate
Full summary, score breakdown and related studies → Original source
CSF-soluble misfolded α-synuclein aggregates (seeds) are readily detected in people with Parkinson's disease by α-synuclein seed amplification assay (synSAA), but identification of seeds associated with multiple system atrophy for diagnostic purposes has proven elusive. 2 key findings →
Design: cohort study Participants: 80 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Hypersynchronization has been proposed as a synaptic dysfunction biomarker in the Alzheimer's disease continuum, reflecting the alteration of the excitation/inhibition balance. 5 key findings →
Design: longitudinal study Participants: 27 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In this study, clinically normal adults with SNAP did not exhibit evidence of elevated tau levels, which suggests that this biomarker construct does not represent amyloid-independent tauopathy. 5 key findings →
Design: longitudinal study Participants: 247 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cerebrospinal fluid neurogranin was increased in patients with Alzheimer's disease dementia (P < 0.001), progressive mild cognitive impairment (P < 0.001) and stable mild cognitive impairment (P < 0.05) compared with controls, and in Alzheimer's disease dementia (P < 0.01) and progressive mild cognitive impairment (P < 0.05) compared with stable mild cognitive impairment. 2 key findings →
Design: longitudinal study Participants: 95 Evidence: moderate
Full summary, score breakdown and related studies → Original source
At baseline, Aβ+ participants showed higher CP FWf, increased white matter hyperintensity (WMH) volume, and decreased diffusion tensor image analysis along the perivascular space (DTI-ALPS). 5 key findings →
Design: cohort study Participants: 216 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD), the leading cause of dementia worldwide, imposes a growing clinical and societal burden, yet no therapies have been proven to alter its progression despite decades of intensive research. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The gut-brain axis explains that changes in the intestinal microbiota influence Alzheimer's disease (AD). 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Research of the human brain metabolism in vivo has largely focused on total glucose use (via fluorodeoxyglucose positron emission tomography) and, until recently, did not examine the use of glucose outside oxidative phosphorylation, which is known as aerobic glycolysis (AG). 2 key findings →
Design: longitudinal study Participants: 42 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a major cause of dementia and cognitive decline. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The microbiota-gut-brain axis (MGBA) is an intricate bidirectional communication network that links intestinal microbiota with the central nervous system (CNS) through immune, neural, endocrine, and metabolic pathways. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
= 0.009). Other neuropathologies were similar across cognitive groups. 4 key findings →
Design: cohort study Participants: 40 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The pathology-based classification of Alzheimer's disease (AD) and other neurodegenerative diseases is a work in progress that is important for both clinicians and basic scientists. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Abnormal forms of prion protein that were found in multiple peripheral tissues were associated with diarrhea, autonomic failure, and neuropathy. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Currently established and employed biomarkers of Alzheimer's disease (AD) predominantly mirror AD-associated molecular and structural brain changes. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Available data, while limited and complicated by selection bias, indicate that exposure to RBT represents the greatest risk factor for CTE pathological features, although clinicopathological correlates and the nature of onset and progression of symptoms are largely unknown. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Early Life Stress (ELS) rodent models have successfully demonstrated sequelae of maternal separation resulting in LOAD-analogous pathology, thereby supporting a role of insulin receptor signalling pertaining to GSK-3beta facilitated tau hyper-phosphorylation and amyloidogenic processing. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The gut microbiota (GM) is a complex, evolutionarily molded ecological system, which contributes to a variety of physiological functions. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Parkinson's disease (PD) is the second most common degenerative disease of the central nervous system (CNS) after Alzheimer's disease. 2 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The loss of excitatory synapses is known to underlie the cognitive deficits in Alzheimer's disease (AD). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Gut microbial metabolites serve as functional mediators of gut–brain communication, linking microbial alterations to neurodegenerative pathology. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Recent data suggest gut microbiota dysbiosis as a contributing factor in neurodegenerative diseases, such as Parkinson's Disease (PD) and Alzheimer's Disease (AD), and these pathologies may manifest via the microbiota-gut-brain-axis, which comprises bidirectional communication through neuroimmune, neuroendocrine, and direct neural pathways such as the vagus nerve. 1 key finding →
Design: longitudinal study Evidence: moderate
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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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