High-fidelity driving simulation provides a unique new source of performance parameters to standardize the assessment of driver fitness. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Our hospice enrollment criteria identified a group with a median survival time of 4 months and a mean survival time of 6.9 months. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings, which are generally consistent with prior reports of reduced hippocampal volume in combat veterans with PTSD, suggest that diminished hippocampal size may be either a consequence of trauma exposure or a risk factor for the development of psychiatric complications following trauma exposure. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Extrahippocampal volume abnormalities were bilateral and occurred in both temporal and extra-temporal cortical regions in TLE, whereas hippocampal deficits were related to the side of the epileptogenic focus. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
High alcohol consumption for long periods of time causes significant hippocampal neurodegeneration in rodents. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microvascular disease, not macroscopic infarction, was the chief substrate of vascular dementia in this series of cases. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Metallothionein-III (MT-III), a brain-specific member of the metallothionein family of metal-binding proteins, is abundant in glutamatergic neurons that release zinc from their synaptic terminals, such as hippocampal pyramidal neurons and dentate granule cells. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) beta-amyloid peptide (Abeta and betaA4) is derived from the amyloid precursor protein (APP) by the subsequent action of the so-far unidentified beta- and gamma-secretases. gamma-secretase, which generates the C-terminus of Abeta, cleaves within the transmembrane domain of APP, preferentially after Abeta-residue 40 (Abeta 40) but also after residue 42 (Abeta 42). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Various mutations in the amyloid protein precursor and presenilin genes can lead to early onset, autosomal Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
36/100
beta-Amyloid precursor protein (beta-APP), the source of the fibrillogenic amyloid beta-peptide (A beta) that accumulates in the brain of victims of Alzheimer's disease, is a multifunctional protein that is widely expressed in the nervous system. beta-Amyloid precursor protein is axonally transported and accumulates in presynaptic terminals and growth cones. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Presenilin-1 (PS1) is the major gene responsible for early-onset familial Alzheimer's disease (FAD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Abeta protofibrils are likely to be intermediates in the in vitro assembly of Abeta amyloid fibrils, but their in vivo role has yet to be determined. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The paired helical filament, which comprises the major fibrous element of the neurofibrillary lesions of Alzheimer's disease, is composed of hyperphosphorylated microtubule-associated protein tau. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We have shown that heat shock induces rapid dephosphorylation of tau in both female and male rats followed by hyperphosphorylation only in female rats. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The majority of cases with familial Alzheimer's disease (FAD) are linked to mutations of the presenilin (PS) genes. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mutant presenilins have been found to cause Alzheimer disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Lithium is one of the most widely used drugs for treating bipolar (manic-depressive) disorder. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease, tau protein becomes hyperphosporylated, which can contribute to neuronal degeneration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The organization and possible functions of basal forebrain and pontine cholinergic systems are reviewed. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tissue deposition of normally soluble proteins as insoluble amyloid fibrils is associated with serious diseases including the systemic amyloidoses, maturity onset diabetes, Alzheimer's disease and transmissible spongiform encephalopathy. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Transcription factors provide the link between early membrane-proximal signalling events and changes in gene expression. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Increasing evidence suggests that oxidative damage to proteins and other macromolecules is a salient feature of the pathology of Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent studies have demonstrated oxidative damage is one of the salient features of Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Oxidative stress is believed to play important roles in neuronal cell death associated with many different neurodegenerative conditions (e.g., Alzheimer's disease, Parkinson's disease, and cerebral ischemia), and it is believed also that apoptosis is an important mode of cell death in these disorders. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We measured 24-hour circadian-rhythm patterns of activity and sleep/wake activity in a group of nursing-home patients (58 women and 19 men with a mean age of 85.7 years). 2 key findings →
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 →