Strategies to control modifiable risk factors should be implemented to decrease the incidence of AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Decreased olfactory function is very common in the older population, being present in >50% of individuals aged between 65 and 80 years and in 62-80% of those >80 years of age. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There is accumulating evidence suggesting that changes in brain perfusion are present long before the clinical symptoms of Alzheimer's disease (AD), perhaps even before amyloid-β accumulation or brain atrophy. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
It is well established that oxidative stress plays a key role in the degenerative neuronal death and progression of Alzheimer's disease (AD), although it is not clear if it is the primary triggering event in the pathogenesis of this disorder. 4 key findings →
Evidence: low
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We propose that brain energy deficit is an important pre-symptomatic feature of Alzheimer's disease (AD) that requires closer attention in the development of AD therapeutics. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Third, we benchmarked the results of our virtual reality episodic memory test against a classical memory test and a subjective daily memory complaint scale. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
This paper reviews the characteristics of sleep disorders found in people at a greater risk of dementia: the elderly adult, patients with mild cognitive impairment (MCI) and those with neurodegenerative diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
43/100
Oxidative stress and endoplasmic reticulum (ER) stress have been associated with Alzheimer's disease (AD) progression. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
43/100
The construct of mild cognitive impairment (MCI) has been proposed to identify patients at risk of developing Alzheimer's disease (AD) in the pre-clinical stage. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
43/100
There are many factors that strongly influence the aetiology, development, and progression of cognitive decline in old age, mild cognitive impairment (MCI), and Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Nerve growth factor (NGF)-dependent cholinergic basal forebrain neurons degenerate during the progression of Alzheimer disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The delayed recall of auditory verbal learning test (AVLT_DR) identified 116 subjects as MCI, resulted in the conversion rate as 44% over the roughly 30-month time interval, missed 7.8% incipient Alzheimer's disease (AD) patients in SCD group who eventually converted to dementia. 3 key findings →
Participants: 95 Evidence: low
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No disease-modifying therapy is currently available for Alzheimer's disease, but therapies are in development, and one may become available in the near future. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
43/100
Mild cognitive impairment (MCI) describes a state of cognitive functioning that is below defined norms, yet falls short of dementia in severity. 1 key finding →
Evidence: low
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Several studies have recently shown that basal ganglia (BG) deterioration leads to distinctive impairments in the domains of syntax, action verbs, and action semantics. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the most common cause of dementia. 1 key finding →
Evidence: low
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Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive decline in multiple cognitive domains. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our findings suggest that restoration of the expression of nuclear-encoded OXPHOS genes in aging could be a viable strategy for blunting AD progression. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Impairment in instrumental activities of daily living (IADL) heralds the transition from mild cognitive impairment (MCI) to dementia and is a major source of burden for both the patient and caregiver. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Apolipoprotein E ε4 (APOE ε4) bring the higher risk of Alzheimer' Disease (AD). 4 key findings →
Participants: 1,610 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Subtle changes in objective spatial navigation ability have been observed in the preclinical stage of Alzheimer disease (AD) cross-sectionally and have been found to predict clinical progression. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma glial fibrillary acidic protein (GFAP) has emerged as a promising biomarker of astrocytic reactivity in preclinical Alzheimer´s Disease (AD). 4 key findings →
Participants: 143 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In this study we investigated impaired awareness of cognitive deficits in patients with mild cognitive impairment (MCI) and Alzheimer's disease (AD). 4 key findings →
Evidence: low
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We investigated possible abnormalities in the retinal nerve fiber layer (RNFL) and macula lutea of patients diagnosed with Alzheimer's disease (AD) and mild cognitive impairment (MCI) and tested for any correlation with the severity of dementia. 4 key findings →
Participants: 72 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Mild Cognitive Impairment (MCI) is a transitional stage between normal aging and dementia and people with MCI are at high risk of progression to dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
From across this tag
10 of the 2,141 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- A deep hybrid CNN-BiLSTM-BiGRU architecture with explainability for mild cognitive impairment detection using EEG
- Mild Cognitive Impairment and Sarcopenia: Effects of Resistance Exercise Training on Neuroinflammation, Cognitive Performance, and Structural Brain Changes
- Efficacy of cognitive rehabilitation therapies for mild cognitive impairment (MCI) in older adults: working toward a theoretical model and evidence-based interventions
- [Patients with mild cognitive impairment and a reduced CSF Aβ₁₋₄₂ protein progress rapidly to Alzheimer's disease]
- Deep and Frequent Phenotyping study protocol: an observational study in prodromal Alzheimer's disease
- Cerebral metabolic changes accompanying conversion of mild cognitive impairment into Alzheimer's disease: a PET follow-up study
- Blood biomarkers for the diagnosis of amnestic mild cognitive impairment and Alzheimer's disease: A systematic review and meta-analysis
- Mild cognitive impairment in the general population: occurrence and progression to Alzheimer disease
- Neuropsychiatric Symptoms in Mild Cognitive Impairment: A Literature Review
- Predicting clinical scores from magnetic resonance scans in Alzheimer's disease
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.
1,034 records (3.7% 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 →