30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Identifying individuals at risk for progression of AD dementia could potentially help to personalize disease management to plan future care. 3 key findings →
Evidence: low
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Amyotrophic lateral sclerosis (ALS) has long been considered to be a purely motor disorder. 5 key findings →
Evidence: low
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Triggering receptor expressed on myeloid cells-2 (TREM2) is a transmembrane receptor of the immunoglobulin superfamily and a crucial signaling hub for multiple pathological pathways that mediate immunity. 4 key findings →
Evidence: low
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The importance of mitogen-activated protein kinase (MAPK) pathway signaling in regulating microglia-mediated neuroinflammation in Alzheimer's disease (AD) remains unclear. 4 key findings →
Evidence: low
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Non-neuronal responses in neurodegenerative disease have received increasing attention as important contributors to disease pathogenesis and progression. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is a chronic neurodegenerative disease characterised by cognitive impairment, behavioural alteration, and functional decline. 4 key findings →
Evidence: low
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Secretases are a group of proteases that are major drug targets considered for the prevention and treatment of Alzheimer's disease (AD). 4 key findings →
Evidence: low
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Microglia are key in the homeostatic well-being of the brain and microglial dysfunction has been implicated in neurodegenerative disorders such as Alzheimer's disease (AD). 4 key findings →
Evidence: low
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PET of β-Amyloid plaques (Aβ) using [ 18 F ] florbetaben ( [ 18 F ] FBB) and [ 18 F ] fluorodeoxyglucose ( [ 18 F ] FDG) increasingly aid clinicians in early diagnosis of dementia, including Alzheimer's disease (AD), frontotemporal disease, dementia with Lewy bodies, and vascular dementia. 4 key findings →
Participants: 40 Evidence: low
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Five overarching themes derived from the interviews were as follows: (a) My life still has value and meaning, (b) I am my own unique individual, (c) I place my trust in other people, (d) The future worries me, and (e) I accept and embrace what life brings. 5 key findings →
Evidence: low
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Per-dyad mean cost savings at 12 months were $2 354 for those who received COPE with a mean difference-in-difference of -$6 667 versus HCBS alone (95% CI: -$15 473, $2 734; not statistically significant). 4 key findings →
Evidence: low
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The agreement between the two measures of dementia differed by age: in 2017, 79.2% of hospital claims for patients aged 66–74 had a diagnosis of dementia compared to older age categories that had dementia noted in over 85% of records. 5 key findings →
Participants: 1,273,348 Evidence: low
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The county clusters with the highest and lowest AD mortality rates were in Washington (WA) and New York (NY), respectively, with other notable high-mortality clusters on the border of Tennessee, Georgia, and Alabama as well as in North Dakota and South Dakota. 5 key findings →
Evidence: low
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Limited data suggest nursing home (NH) Alzheimer's special care units (ASCUs) may improve care and outcomes among residents with dementia. 5 key findings →
Design: cross-sectional Participants: 13,207 Evidence: low
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Abbreviations Aβ: β-amyloid; AD: Alzheimer disease; AIF1/IBA1: allograft inflammatory factor 1; ALP: autophagy-lysosomal pathway; APP: amyloid beta precursor protein; ATP6V1B1/V-ATPase V1b1: ATPase H+ transporting V1 subunit B1; AVs: autophagy vacuoles; BAF: bafilomycin A 1 ; CFC: contextual/cued fear conditioning assay; CHX: Ca 2+ /H + exchanger; CTF-β: carboxy-terminal fragment derived from β-secretase; CTSD: cathepsin D; fAD: familial Alzheimer disease; GFAP: glial fibrillary acidic protein; LAMP1: lysosomal associated membrane protein 1; LTP: long-term potentiation; MCOLN1/TRPML1: mucolipin 1; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MAPT: microtubule associated protein tau; MWM: Morris water maze; NFT: neurofibrillary tangles; PFC: prefrontal cortex; PSEN1: presenilin 1; SQSTM1/p62: sequestosome 1; TBS: theta burst stimulation; TEM: transmission electronic microscopy; TPCN2/TPC2: two pore segment channel 2; WT: wild-type; V-ATPase: vacuolar type H + -ATPase. 1 key finding →
Evidence: low
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We previously demonstrated that PNA5, a novel glycosylated angiotensin 1-7 (Ang-(1-7)) Mas receptor (MasR) agonist peptide, is an effective therapy to rescue cognitive impairment in our preclinical model of VCID. 5 key findings →
Participants: 15 Evidence: low
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SNfL was perceived as useful in 53% (n = 58) of the cases. 3 key findings →
Evidence: moderate
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Overall, the study with the same protocol is going as expected with no serious AE or any major protocol deviation. 2 key findings →
Participants: 150 Evidence: high
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Increasing age (especially >60 years) may be the most important risk factor for severe outcomes. 2 key findings →
Evidence: low
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Chronic cerebral hypoperfusion (CCH) is regarded as a high-risk factor for cognitive decline in vascular dementia (VaD). 4 key findings →
Evidence: low
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Here, we found a close association of the metabolic reconfiguration of microglia with increased hippocampal glucose uptake on [ 18 F]fluorodeoxyglucose (FDG) PET. 4 key findings →
Evidence: low
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Amyloidogenicity and vascular dysfunction are the key players in the pathogenesis of Alzheimer's disease (AD), involving dysregulated cellular interactions. 4 key findings →
Evidence: low
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Patients with essential tremor (ET) frequently develop concurrent dementia, which is often assumed to represent co-morbid Alzheimer disease (AD). 4 key findings →
Participants: 13 Evidence: low
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Annual Wellness Visit utilization was associated with an increased probability of new dementia diagnosis with effects varying by racial group (categorized as white, black, Hispanic/Latino, or Asian based on Social Security Administration data). 5 key findings →
Evidence: low
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Associations of neighbourhood NO2 level, walkability, public open space and social fragmentation with dementia incidence and estimated future risk of dementia were statistically significant, indicating the potential to reduce the risk through changes in built and social environments. 3 key findings →
Participants: 25,511 Evidence: low
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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.
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