Loss of physiological microglial function may increase the propagation of neurodegenerative diseases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Loss of physiological microglial function may increase the propagation of neurodegenerative diseases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 →
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Age-related cognitive decline is likely promoted by accumulated brain injury due to chronic conditions of aging, including neurodegenerative and vascular disease. 4 key findings →
Participants: 749 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Mutations in the CHCHD10 gene have been recently identified in a large family with a complex phenotype variably associating frontotemporal dementia (FTD) with amyotrophic lateral sclerosis (ALS), cerebellar ataxia, myopathy, and hearing impairment. 1 key finding →
Participants: 115 Evidence: low
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Individuals with Down syndrome (DS) are more likely to experience earlier onset of multiple facets of physiological aging. 3 key findings →
Participants: 46 Evidence: low
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Cerebrospinal fluid (CSF) neurofilament light (NfL) concentration has reproducibly been shown to reflect neurodegeneration in brain disorders, including Alzheimer's disease (AD). 3 key findings →
Participants: 227 Evidence: low
Full summary, score breakdown and related studies → Original source
The objective of this study was to determine the differential mapping of plasma biomarkers to postmortem neuropathology measures. 2 key findings →
Participants: 64 Evidence: low
Full summary, score breakdown and related studies → Original source
Synaptic dysfunction is the best anatomical correlate of early cognitive impairment in Alzheimer's disease (AD). 4 key findings →
Participants: 210 Evidence: low
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Synaptic dysfunctions precede cognitive decline in Alzheimer's disease by decades, affect executive functions, and can be detected by quantitative electroencephalography (qEEG). 4 key findings →
Participants: 20 Evidence: low
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Different clinical variants of probable Alzheimer's disease (AD) share underlying plaques and tangles but show distinct atrophy patterns. 2 key findings →
Participants: 52 Evidence: low
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Mutations of 3 causative genes, namely presenilin 1 (PSEN1), presenilin 2 (PSEN2), and amyloid precursor protein (APP), have been identified as the major causes of early-onset familial Alzheimer's disease (EOFAD). 5 key findings →
Participants: 32 Evidence: moderate
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Homozygous mutations in TREM2 have been recently identified by exome sequencing in families presenting with frontotemporal dementia (FTD)-like phenotype. 2 key findings →
Participants: 175 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The objective of this study was to examine the distribution and severity of tau-PET binding in cognitively normal adults with preclinical Alzheimer's disease as determined by positive beta-amyloid PET. 18 F-AV-1451 tau-PET data from 109 cognitively normal older adults were processed with 34 cortical and 9 subcortical FreeSurfer regions and averaged across both hemispheres. 1 key finding →
Participants: 25 Evidence: moderate
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We examined the characteristics of individuals with biomarker evidence of tauopathy but without β-amyloid (Aβ) (A-T+) in relation to individuals with (A+T+) and without (A-T-) evidence of Alzheimer's disease (AD). 5 key findings →
Participants: 316 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is associated with reduced temporo-parietal cerebral blood flow (CBF). 4 key findings →
Participants: 156 Evidence: low
Full summary, score breakdown and related studies → Original source
(11)C-Pittsburgh compound B (PiB) is a positron emission tomography (PET) tracer designed to bind to amyloid-β (Aβ) plaques, one of the hallmarks of Alzheimer's disease (AD). 3 key findings →
Participants: 237 Evidence: low
Full summary, score breakdown and related studies → Original source
In region-of-interest (ROI) analyses, we found modest but statistically significant declines in FDG ratio in most cortical and subcortical regions as a function of age. 4 key findings →
Participants: 806 Evidence: low
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Astrocytes contribute to a variety of functions in the brain, including homeostasis, synapse formation, plasticity, and metabolism. 3 key findings →
Evidence: moderate
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Although amyloid plaques and neurofibrillary pathology play important roles in Alzheimer disease (AD), our understanding of AD is incomplete, and the contribution of microglia and iron to neurodegeneration is unknown. 1 key finding →
Evidence: low
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Older women with low estradiol levels were more likely to experience decline in global cognitive function and verbal memory, and a similar trend was observed for verbal memory in men. 4 key findings →
Evidence: low
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Identifying individuals destined to develop Alzheimer's dementia within time frames acceptable for clinical trials constitutes an important challenge to design studies to test emerging disease-modifying therapies. 5 key findings →
Evidence: low
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Sleep, EEG and mental function variables were studied in 44 subjects diagnosed as having probable senile dementia of the Alzheimer's type (SDAT) and 22 controls matched for age and minimal depression. 3 key findings →
Participants: 44 Evidence: low
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Increased peripheral and central nervous system cortisol levels have been reported in Alzheimer's disease (AD) and may reflect dysfunction of cerebral components of the hypothalamic-pituitary-adrenal (HPA) axis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The aim of this study was to investigate the dynamics of four of the most validated biomarkers for Alzheimer's disease (AD), cerebro-spinal fluid (CSF) Abeta 1-42, tau, hippocampal volume, and FDG-PET, in patients at different stage of AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events