Proteins exist as diverse proteoforms resulting from a combination of genetic variation, alternative splicing, and post-translational modifications. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
43/100
Filamentous tau inclusions in neurons and glia are neuropathological hallmarks of sporadic and familial tauopathies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We conclude with an interdependent list of challenges that must be collaboratively addressed before these endpoints are widely adopted. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Early detection and timely intervention play a vital role in the effective management of Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We quantified the amount of amyloid beta-peptide (Abeta) immunoreactivity as well as amyloid deposits in a large cohort of transgenic mice overexpressing the V717F human amyloid precursor protein (APP(V717F+/-) TG mice) with no, one, or two mouse apolipoprotein E (Apoe) alleles at various ages. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Human γ-secretase is an intra-membrane protease that cleaves many different substrates. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
After the authors controlled for demographic characteristics and dementia severity, both estimates of premorbid intellectual ability were inversely correlated with cerebral metabolism in the prefrontal, pre-motor, and left superior parietal association regions. 4 key findings →
Participants: 46 Evidence: low
Full summary, score breakdown and related studies → Original source
Aducanumab (BIIB037) is a human monoclonal antibody selective for aggregated forms of beta-amyloid peptide being investigated as a disease-modifying treatment for AD. 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source
43/100
Three deaths have been reported related to treatment with lecanemab.6 Patients receiving DMT require frequent monitoring with MRI brain scans (four or more per year), as there is a high rate of clinically significant amyloid-related imaging abnormalities (ARIA), both brain oedema (ARIA-E) and macro- and microhaemorrhages (ARIA-H). 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease is the most common form of dementia, and epidemiological studies support that type 2 diabetes (T2D) is a major contributor. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
However, the fibrils in primary amyloidosis (AL) consist of the variable portion of a monoclonal light chain (κ or λ); secondary amyloidosis (AA) fibrils consist of protein A, a non-immunoglobulin; familial amyloidosis fibrils are usually composed of mutated transthyretin (prealbumin); senile systemic amyloid fibrils consist of normal transthyretin; and amyloid associated with long-term dialysis consists of β2-microglobulin. 5 key findings →
Participants: 60 Evidence: low
Full summary, score breakdown and related studies → Original source
Studies of the association of high blood pressure (BP) with dementia are not consistent. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
In this multicenter study, the clinical efficacy of citalopram was investigated in 98 patients with moderate AD/SDAT or VD using a combined double-blind and open technique with placebo and citalopram. 2 key findings →
Participants: 98 Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
Physostigmine (0.25 mg-1 mg), arecoline (2 and 4 mg) and saline were administered intravenously over 30 minutes in a randomized double blind design to 11 patients with a clinical diagnosis of Alzheimer presenile dementia. 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source
Fifteen cases were identified (14 men). All had clear histories of dream enactment behavior, and 10 had RBD confirmed by polysomnography. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our earlier studies using the Consortium to Establish a Registry of Alzheimer's Disease neuropsychological battery showed that delayed recall was a highly sensitive indicator of early Alzheimer's disease. 1 key finding →
Participants: 49 Evidence: low
Full summary, score breakdown and related studies → Original source
A stress and coping model was used to study predictors of individual differences in caregiver adaptation. 2 key findings →
Participants: 54 Evidence: low
Full summary, score breakdown and related studies → Original source
Clinical and neuropathologic data in 45 patients with Parkinson's disease (PD) were compared. 3 key findings →
Participants: 45 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) could result from a multifactorial process involving both genetic predisposition and exposure to environmental factors like pesticides. 3 key findings →
Participants: 70 Evidence: low
Full summary, score breakdown and related studies → Original source
Essential oils are promising as environmentally friendly and safe sources of pesticides for human use. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent extensive evidence suggests that ambient fine particulate matter (PM2.5, with an aerodynamic diameter ≤2.5 μm) may be neurotoxic to the brain and cause central nervous system damage, contributing to neurodevelopmental disorders, such as autism spectrum disorders, neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease, and mental disorders, such as schizophrenia, depression, and bipolar disorder. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The age-adjusted smoking prevalence of adults with mental illness or serious psychological distress ranged from 34.3% (phobias or fears) to 59.1% (schizophrenia) compared with 18.3% of adults with no such illness. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Participants who drank no alcohol at midlife and those who drank alcohol frequently were both twice as likely to have mild cognitive impairment in old age as those participants who drank alcohol infrequently. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Globally, in 2019, there were nearly 10 million deaths and 349 million DALYs due to neurological disorders. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Extracellular neuritic plaques composed of amyloid‑β (Aβ) protein and intracellular neurofibrillary tangles containing phosphorylated tau protein are the two hallmark proteins of Alzheimer's disease (AD), and the separate neurotoxicity of these proteins in AD has been extensively studied. 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →