27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Although hypertension is well known as a cause of vascular dementia (VaD), recent findings highlight the role of hypertension in the pathogenesis of Alzheimer's disease (AD) as well as mild cognitive impairment (MCI). 1 key finding →
Evidence: low
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However, recent data suggest that the risk of adverse effects may offset the benefits of atypical agents in patients with dementia. 5 key findings →
Evidence: low
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In general, there was only a moderate alteration of gene expression in ADAM10 overexpressing mice. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Stem cells are central to the development and maintenance of many tissues. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In the literature it is commonly reported that several spatial abilities decline with normal aging, even though such a decline is not uniform. 1 key finding →
Evidence: low
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Amyloid precursor protein (APP) can be proteolytically processed along two pathways, the amyloidogenic that leads to the formation of the 40-42 amino acid long Alzheimer-associated amyloid β (Aβ) peptide and the non-amyloidogenic in which APP is cut in the middle of the Aβ domain thus precluding Aβ formation. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral amyloid angiopathy (CAA) refers to the specific deposition of amyloid fibrils in the leptomeningeal and cerebral blood vessel walls, often causing secondary vascular degenerative changes. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) has become a matrix for biomarker discovery and development in recent years. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
There are two types of dementia with early onset: (i) presenile dementias; and (ii) senile dementias with early onset. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cholinesterase inhibitors (ChEIs) were introduced in the therapy of Alzheimer Disease (AD) in the nineteen nineties with great expectations. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Emerging science suggests that aerobic exercise might modify the pathophysiology of Alzheimer's disease (AD) and improve cognition. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
There is a cluster of risk factors for Type 2 diabetes and vascular disease that include high blood glucose, obesity, high blood pressure, increased blood triacylglycerols and insulin resistance. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Depression and cognitive impairment are both common conditions in old age, and frequently occur together. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research on the impact of the built environment in long-term care settings continues to grow. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
You have been called to the emergency room to evaluate an elderly nursing home patient sent for consultation who has ischemic gangrene of the right foot. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Activation of astrocytes has been known to be associated with amyloid-beta (Abeta) deposit and production of pro-inflammatory cytokines and chemokines that lead to neuronal cell death in the pathogenesis of Alzheimer disease (AD). 5 key findings →
Evidence: low
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The finding of postmortem susceptibility-weighted changes in the cerebral cortex of patients with cerebral amyloidosis with a human 7.0-T MR imaging system opens up the possibility of obtaining in vivo radiologic evidence of cerebral amyloid beta deposition. 1 key finding →
Evidence: low
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Chronic cerebral hypoperfusion (CCH) increases the risk of Alzheimer disease (AD) through several biologically plausible pathways, but the relationship between CCH and the development of AD remains uncertain. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is the leading cause of dementia. 4 key findings →
Participants: 53 Evidence: low
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The aim of this study was twofold: to compare the functional levels of elderly awaiting nursing home placement and nursing home residents, and to compare their nurses' physical and psychological workloads. 5 key findings →
Participants: 36 Evidence: low
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder with characteristic neuropathological changes of the brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mitochondrial stress is one of the early features of Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The amyloid hypothesis (AH) of Alzheimer's disease (AD) posits that the fundamental cause of AD is the accumulation of the peptide amyloid beta (Aβ) in the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Nitric oxide (NO), plays multiple roles in the nervous system. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aggregation and cleavage are two hallmarks of Tau pathology in Alzheimer disease (AD), and abnormal fragmentation of Tau is thought to contribute to the nucleation of Tau paired helical filaments. 1 key finding →
Evidence: low
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 →