In nondemented individuals, entorhinal cortex atrophy is associated with risk of Alzheimer disease. 3 key findings →
Participants: 58 Evidence: low
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27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
In nondemented individuals, entorhinal cortex atrophy is associated with risk of Alzheimer disease. 3 key findings →
Participants: 58 Evidence: low
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Microstructural white matter changes are present in cognitively normal individuals in the pre-aMCI stage, and may serve as a potential imaging marker of early AD-related brain changes. 1 key finding →
Participants: 193 Evidence: low
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Spatially distinct neurodegeneration is associated with Aβ and tau pathology in preclinical AD. 5 key findings →
Participants: 188 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Histologic studies show that the amygdala is affected by Alzheimer disease (AD) pathology, and its medial aspect is the most involved. 1 key finding →
Participants: 19 Evidence: low
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This study provides evidence for heterogeneous pathologic substrates and possibly different pathophysiologic mechanisms underlying MRI-observed cortical microbleeds in the context of advanced CAA and Alzheimer disease. 1 key finding →
Evidence: low
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This effect is independent of baseline neuropsychological and MRI predictors. 3 key findings →
Participants: 31 Evidence: low
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Subjects were 233 older Catholic clergy in the Religious Orders Study, who underwent detailed annual evaluations, including neuropsychological testing, and brain autopsy at time of death (mean age 86 years, 45% men). 2 key findings →
Evidence: low
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These are the first AD incidence rates to be reported from the Indian subcontinent, and they appear to be among the lowest ever reported. 3 key findings →
Evidence: moderate
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NIFID is a neuropathologically distinct, clinically heterogeneous variant of frontotemporal dementia (FTD) that may include parkinsonism or MND. 1 key finding →
Evidence: low
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We studied the prevalence of different types of dementia in an elderly population in Stockholm, Sweden, in relation to age, sex, and education. 1 key finding →
Evidence: low
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We evaluated the Lund-Manchester research criteria (LMRC) for frontotemporal dementia (FTD). 3 key findings →
Participants: 30 Evidence: low
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Patients with autopsy-confirmed low-, intermediate-, and high-likelihood DLB, according to the probability statement recommended by the third report of the DLB Consortium, and antemortem MRI, were identified (n = 75). 3 key findings →
Participants: 75 Evidence: low
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Current concepts of the pathogenesis of Parkinson's disease (PD) center on the formation of reactive oxygen species and the onset of oxidative stress leading to oxidative damage to substantia nigra pars compacta. 2 key findings →
Evidence: low
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These findings indicate that in patients with MCI, the patient's lack of awareness of functional deficits identified by informants strongly predicts a future diagnosis of AD. 5 key findings →
Evidence: low
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Abnormalities of the P600 or N400 in mild cognitive impairment are associated with an increased risk of subsequent conversion to Alzheimer disease (AD). 3 key findings →
Participants: 32 Evidence: low
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Cerebral amyloid angiopathy (CAA) is currently diagnosed using MRI-based Boston criteria. 4 key findings →
Design: cohort study Participants: 102 Evidence: moderate
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Prior studies report that subjects with neuropathologic evidence of AD and concomitant brain infarcts had poorer cognitive function and higher frequency of dementia than those with AD alone. 4 key findings →
Participants: 74 Evidence: low
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Since the discovery of CSF1R gene mutations in families with hereditary diffuse leukoencephalopathy with spheroids in 2012, more than 70 different mutations have been identified around the world. 4 key findings →
Evidence: low
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< 0.001). This study suggests 2 molecular pathways underlying CAA, with a larger effect size for the pathway including SFRP1 and APOE protein and C-terminally truncated Aβ before position 40. 2 key findings →
Design: cross-sectional Evidence: low
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Superficial white matter (SWM), containing short-range association connections beneath the cortex, has been affected in mild cognitive impairment and AD, with gaps in understanding the disease's early stages. 3 key findings →
Evidence: low
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= 0.029). Despite the absence of overt nOH, patients with DLB show covert dysautonomia encompassing adrenergic, parasympathetic, and sudomotor dysfunction, highlighting the importance of standardized autonomic evaluation. 3 key findings →
Design: cohort study Evidence: moderate
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= 0.02). Lifetime exposure to cognitive enrichment was related to lower risk of AD dementia and a slower rate of cognitive decline, including after adjustment for common ADRD pathologies, indicating higher resilience provided by lifetime enrichment. 2 key findings →
Design: longitudinal study Evidence: moderate
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= 0.038) over time. Physical activity was associated with less synaptic dysfunction and cognitive activity with less synaptic dysfunction and lower amyloid burden over time, albeit effect sizes were small. 2 key findings →
Design: longitudinal study Evidence: moderate
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= 0.025) over 3 years. NfL was not significantly associated with any MRI cSVD marker. 5 key findings →
Design: longitudinal study Evidence: moderate
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Among older adults, MeDi adherence was associated with less brain atrophy, with an effect similar to 5 years of aging. 5 key findings →
Design: cross-sectional 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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →