Hippocampal and serum irisin levels were progressively reduced in CCH mice. 5 key findings →
Participants: 212 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Hippocampal and serum irisin levels were progressively reduced in CCH mice. 5 key findings →
Participants: 212 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer’s disease (AD), the leading cause of senile dementia, lacks effective therapies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Herpes Zoster (HZ), caused by the reactivation of the varicella-zoster virus (VZV), is a common infectious disease. 2 key findings →
Design: cohort study Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Plasma pTau217 levels serve as a scalable, non-invasive marker of AD-pathology across Lewy body diseases, PSP/CBS, and MCI/CU populations. 2 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
-heterozygous human brain tissue was reactivated in response to neuroinflammation caused by exposure to other pathogens. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Genome-wide association studies have led to numerous genetic loci associated with Alzheimer's disease (AD). 2 key findings →
Participants: 2,247 Evidence: low
Full summary, score breakdown and related studies → Original source
Synaptic dysfunction is increasingly recognized as an early and biologically relevant component of α-synucleinopathies. 5 key findings →
Design: systematic review Evidence: high
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Animal studies indicate that Dang Gui Shao Yao San (DGSYS) may enhance cognitive function in VaD models through mechanisms such as antioxidation and the enhancement of cerebral blood flow. 4 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Research on cognitive impairment (CI) has increasingly focused on the central nervous system, identifying numerous neuronal targets and circuits of relevance for CI pathogenesis and treatment. 1 key finding →
Design: systematic review Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
This study evaluated neuronal changes related to Alzheimer's disease using specific immunocytochemical methods (AT8) before the actual formation of neurofibrillary tangles and neuropil threads. 3 key findings →
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Ten participants with AD (5 male and 5 female; mean [SD] age, 72.7 [6.3] years; 10 [100%] β-amyloid positive) were compared with 11 participants who were cognitively normal (5 male and 6 female; mean [SD] age, 72.9 [8.7] years; 11 [100%] β-amyloid negative). 4 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings suggest that the proposition that synaptic markers can predict cognitive decline in AD, should be extended to Lewy body diseases. 4 key findings →
Participants: 129 Evidence: low
Full summary, score breakdown and related studies → Original source
We investigated the incidence and extent of Lewy body (LB)-related alpha-synucleinopathy (LBAS) in the olfactory bulb (OB) in 320 consecutive autopsy patients from a general geriatric hospital (mean age, 81.5 +/- 8.5 years). 1 key finding →
Participants: 102 Evidence: low
Full summary, score breakdown and related studies → Original source
Early-phase FBB acquisitions correlate on a relative quantitative and visual level with FDG PET scans, irrespective of the amyloid plaque density assessed in late FBB imaging. 3 key findings →
Participants: 33 Evidence: low
Full summary, score breakdown and related studies → Original source
HIGHLIGHTS: Different plasma phosphorylated tau (p-tau) species reflect different pathological processes of Alzheimer's disease (AD), with p-tau231 showing the greatest association with the earliest increases in brain amyloid beta (Aβ) accumulation, while p-tau217 shows greater association with both brain Aβ and early tau pathology, and other p-tau and tau fragment species show greater association with later stages of brain tau pathology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
WMH are only weakly and inconsistently associated with cognitive decline, which may be explained by heterogeneity of the underlying neuropathological substrates. 5 key findings →
Participants: 104 Evidence: low
Full summary, score breakdown and related studies → Original source
The present patients with positive GFAP-immunoglobulin G are highly similar to autoimmune GFAP astrocytopathy, described in a recent report. 3 key findings →
Participants: 19 Evidence: low
Full summary, score breakdown and related studies → Original source
This work demonstrates a mobile version of VisMET capable of estimating the presence of cognitive impairment. 1 key finding →
Participants: 250 Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (apoE) is associated with Alzheimer's neurofibrillary tangles and beta-amyloid protein in senile plaques. 3 key findings →
Participants: 91 Evidence: low
Full summary, score breakdown and related studies → Original source
There is an urgent need to develop molecular biomarkers of brain age in order to advance our understanding of age related neurodegeneration. 3 key findings →
Participants: 700 Evidence: low
Full summary, score breakdown and related studies → Original source
The neocortex is disproportionately expanded in human compared with mouse 1,2 , both in its total volume relative to subcortical structures and in the proportion occupied by supragranular layers composed of neurons that selectively make connections within the neocortex and with other telencephalic structures. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This transcriptomic network analysis of 19 brain regions provides a comprehensive assessment of the critical molecular pathways associated with AD pathology and offers new insights into molecular mechanisms underlying selective regional vulnerability to AD at different stages of the progression of cognitive compromise and development of the canonical neuropathological lesions of AD. 5 key findings →
Participants: 125 Evidence: low
Full summary, score breakdown and related studies → Original source
Recent studies indicate that the adaptive immune system plays a role in Lewy body dementia (LBD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Elevated FTP-PET reflects Braak IV or greater neuropathology. 3 key findings →
Participants: 26 Evidence: low
Full summary, score breakdown and related studies → Original source
This evaluation shows an [ 18 F]MK-6240 distribution in concordance with postmortem studies and that simplified quantitative approaches such as the SUVR offer valid estimates of neurofibrillary tangle load 90 min post injection. [ 18 F]MK-6240 is a promising tau tracer with the potential to be applied in the disease diagnosis and assessment of therapeutic interventions. 2 key findings →
Participants: 14 Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 6,970 studies in this tag that have a study page, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →