Amyloid-beta (Abeta) accumulation in the brain extracellular space is a hallmark of Alzheimer's disease.
Full summary, score breakdown and related studies → Original source Free full text
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The conservation of sleep across all animal species suggests that sleep serves a vital function.
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MAF supplementation improved cognitive function, especially after 6 months, in elderly people undergoing rehabilitation. 4 key findings →
Design: randomized controlled trial Evidence: low
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Cardiac 123I-MIBG findings are similar among idiopathic RBD and the syndromes of PD and DLB, but differ from those of PSP and MSA. 4 key findings →
Design: cross-sectional Participants: 95 Evidence: low
Full summary, score breakdown and related studies → Original source
Nutritional supplementation is emerging as a promising strategy to support clinical management of early Alzheimer's disease (AD), partly through modulation of the intestinal microbiome via the microbiota-gut-brain axis. 1 key finding →
Participants: 22 Evidence: low
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Compared to CN counterparts, patients with MCI have higher proportion of families Sclerotiniaceae, Phaffomyceteceae, Trichocomaceae, Cystofilobasidiaceae, Togniniaceae and genera Botrytis, Kazachstania, Phaeoacremonium and Cladosporium and lower abundance of Meyerozyma. 2 key findings →
Evidence: high
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Alzheimer's disease (AD) is a major public health concern in societies with increasingly ageing populations. 3 key findings →
Design: longitudinal study Evidence: moderate
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The microbiota-gut-brain axis (MGBA) is increasingly recognized as a critical regulator of brain health, influencing both neurodevelopment and age-related neurological decline. 5 key findings →
Evidence: low
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The gut-brain axis plays a critical role in maintaining neuronal integrity and influencing the progression of Alzheimer's disease (AD). 2 key findings →
Evidence: low
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The Ketogenic Diet (KD) improves memory and longevity in aged C57BL/6 mice. 5 key findings →
Evidence: low
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Alzheimer's disease (AD) is the primary cause of dementia in older individuals, exhibiting an increasing incidence worldwide. 3 key findings →
Evidence: low
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The Maillard reaction is a simple but ubiquitous reaction that occurs both in vivo and ex vivo during the cooking or processing of foods under high-temperature conditions, such as baking, frying, or grilling. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the major cause of dementia, characterized by the presence of amyloid-beta plaques and neurofibrillary tau tangles. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Neurovascular integrity, including cerebral blood flow (CBF) and blood-brain barrier (BBB) function, plays a major role in determining cognitive capability. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The gut microbiota has been linked to various neurological disorders via the gut-brain axis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Metabolic endotoxemia is a condition in which blood lipopolysaccharide (LPS) levels are elevated, regardless of the presence of obvious infection. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Gut microbiome is a community of microorganisms in the gastrointestinal tract. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Nutrition is known to play an important role in the pathogenesis of Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
An epidemic of age-associated cognitive decline, most commonly ascribed to neurodegenerative conditions such as Alzheimer's and Parkinson's disease, is causing healthcare costs to soar and devastating caregivers. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The microbiota-gut-brain axis refers to the intricate bidirectional communication between commensal microorganisms residing in the digestive tract and the central nervous system, along neuroendocrine, metabolic, immune, and inflammatory pathways. 5 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
Hundreds of billions of commensal microorganisms live in and on our bodies, most of which colonize the gut shortly after birth and stay there for the rest of our lives. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Given the complex bidirectional communication system that exists between the gut microbiome and the brain, there is growing interest in the gut microbiome as a novel and potentially modifiable risk factor for Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Animal models provide consistency and validity of research results from in vitro studies or studies with rodents. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Vitamin D (Vt. D) is one of the vital hormone having multiple functions in various tissues, including brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
There is growing evidence of the involvement of advanced glycation end products (AGEs) in the pathogenesis of neurodegenerative processes including Alzheimer's disease (AD) and their function as a seed for the aggregation of Aβ, a hallmark feature of AD. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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.
What this library is — and isn't
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 →