In humans, age-related memory impairments begin in mid-life and cognitive weakening continues with advancing age. 4 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.
Prototypes for two devices (armband and electronic notepad) were developed. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Medical conditions overall, do impact the fitness to drive of older drivers; however, the crash risk tends to be only slightly to moderately increased. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Inflammation is a critical component of the pathogenesis of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
36/100
We have previously reported anti-amyloidogenic effects of leptin using in vitro and in vivo models and, more recently, demonstrated the ability of leptin to reduce tau phosphorylation in neuronal cells. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Air pollution has been implicated as a chronic source of neuroinflammation and reactive oxygen species (ROS) that produce neuropathology and central nervous system (CNS) disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Between 1980 and 1987, the number of hospital discharges with total hip replacement (THR) increased by more than 90%, while total hospital discharges fell by more than 10%. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Early-phase tau mutant organoids showed elevated tau, hyperdynamic microtubules, and neuronal hyperexcitability, partially reversible by tau reduction. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These findings suggest that sexual differentiation in early life has modest effects on adult development of AD in females, a relationship that appeared stronger in the context of APOE4 . 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The onset and sustenance of Alzheimers and Parkinsons is solely dependent on the driving power of the immune cytokine interleukin-1 beta (IL-1β), arising from neuronal distress and release of sAPPα, which activates microglia for synthesis and release of IL-1β driving synthesis of βAPP, Aβ plaques and synthesis and activation of MAPKp38 for phosphorylation of tau for neurofibrillary tangle formation in Alzheimers and for a-synuclein for formation of Lewy bodies in Parkinsons. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Beyond their role in energy production, mitochondria also interact with other organelles through forming membrane contacts that serve as central hubs of cellular metabolism and signaling. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We evaluated known AD-associated loci (Bellenguez et al. 2022) and 27 loci reached nominal significance (p < 0.05) in at least one cognitive domain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dementia is a syndrome characterised by the development of multiple cognitive deficits and behavioural changes that significantly interfere with various aspects of life. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27/100
Dementia encompasses a group of progressive neurodegenerative disorders marked by cognitive, behavioural, and functional decline, underpinned by complex neurobiological processes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Lecanemab ist eine Anti-Amyloid-Antikörper-Therapie, die entwickelt wurde, um toxische Amyloid-Plaques zu beseitigen und das Fortschreiten der Alzheimer-Krankheit zu verlangsamen. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
25/100
This chapter examines how grocery stores and Whole Foods Market in particular, have driven the rise of precautionary consumption. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Genome-wide association studies (GWAS) typically represent Alzheimers disease (AD) risk loci by a single lead SNP, although the lead SNP may capture only part of the genetic variation at a locus. 3 key findings →
Participants: 493 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Structured AbstractO_ST_ABSINTRODUCTIONC_ST_ABSThe Collaborative Amish Aging and Memory Project (CAAMP) is an ongoing longitudinal study spanning multiple sites, focused on cognitive function and age-related traits in Midwestern Amish (Ohio and Indiana) communities. 5 key findings →
Design: prospective cohort Participants: 3,978 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our results demonstrate that the multi-modal classifier achieved strong classification performance (accuracy = 68.64%; precision = 73.97%; F1-score=74.48%), with the highest recall (76.39%) from a model incorporating demographics and driving features, and prediction performance (accuracy = 70.48%; precision = 71.88%; F1-score = 74.80%, recall = 77.97%). 1 key finding →
Participants: 118 Evidence: low
Full summary, score breakdown and related studies → Original source
16/100
Cerebral small vessel disease (CSVD) is strongly linked to metabolic risk factors and represents a major cause of vascular cognitive impairment and dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Early neuronal hyperexcitability is a hallmark of Alzheimer’s disease (AD) and correlates with cognitive decline. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) flow and the glymphatic system are essential for maintaining brain homeostasis, yet the precise mechanisms driving their profound failure in Alzheimer’s disease (AD) remain largely elusive. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) flows through perivascular spaces (PVSs) surrounding brain vasculature, and impaired flow has been linked to neurodegenerative diseases such as Alzheimer’s. However, the mechanisms driving CSF flow and its oscillatory dynamics remain poorly understood. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although Alzheimer’s disease (AD) and glioblastoma (GBM) share common aging-related risk factors, they lead to opposite cellular fates—neurodegeneration versus uncontrolled proliferation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This structural configuration shields the scaffold from calpain-mediated cleavage, reconfiguring FLNA into an active motility engine driving invasive lamellipodia but stalls proteolytic processing and forces an absolute loss of the nuclear FLNA-90 tumor-suppressor brake, unleashing uninhibited c-Myc oncogenic transcription. 5 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 →