Most proteins must fold into defined three-dimensional structures to gain functional activity. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Oxidative stress is known to play an important role in the pathogenesis of a number of diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Oxidative stress is proposed as a regulatory element in ageing and various neurological disorders. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is one of the most prevalent neurodegenerative diseases, characterized by impaired cognitive function due to progressive loss of neurons in the brain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Stress proteins located in the cytosol or endoplasmic reticulum (ER) maintain cell homeostasis and afford tolerance to severe insults. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Decades of research indicate mitochondria from Alzheimer's disease (AD) patients differ from those of non-AD individuals. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A variable combination of developmental delay, retinitis pigmentosa, dementia, seizures, ataxia, proximal neurogenic muscle weakness, and sensory neuropathy occurred in four members of a family and was maternally transmitted. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Ensuring cellular protein homeostasis, or proteostasis, requires precise control of protein synthesis, folding, conformational maintenance, and degradation. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is conceptualized as a progressive consequence of two hallmark pathological changes in grey matter: extracellular amyloid plaques and neurofibrillary tangles. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Increasing numbers of individuals, particularly the elderly, suffer from neurodegenerative disorders. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Stress is critically involved in the development and progression of disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Caspases mediate essential key proteolytic events in inflammatory cascades and the apoptotic cell death pathway. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although strong findings have shown the positive effects of GH/IGF-1 administration on neuroregeneration in animal models, a very limited number of clinical studies have been conducted in humans. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
The use of essential oils (EOs) and their components is known since long in traditional medicine and aromatherapy for the management of various diseases, and is further increased in the recent times. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apathy is a debilitating syndrome associated with many neurological disorders, including several common neurodegenerative diseases such as Parkinson's disease and Alzheimer's disease, and focal lesion syndromes such as stroke. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Post-translational modifications (PTMs) on tau have long been recognized as affecting protein function and contributing to neurodegeneration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurodegenerative disorder characterized clinically by severe cognitive deficits and pathologically by amyloid plaques, neuronal loss, and neurofibrillary tangles. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Down's syndrome (DS) or trisomy 21 is the most common genetic cause of mental retardation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The cerebral cortex of Alzheimer's and Down syndrome patients is characterized by the presence of protein deposits in neurofibrillary tangles, neuritic plaques, and neuropil threads. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is the most common cause of progressive intellectual failure in aged humans. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The typical abnormalities observed in the brain of Alzheimer's disease (AD) patients include synaptic alterations, neuronal death, brain inflammation, and the accumulation of protein aggregates in the form of amyloid plaques and neurofibrillary tangles. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Oxidative stress develops as a response to injury and reflects a breach in the cell's antioxidant capacity. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Human hereditary cerebral hemorrhage with amyloidosis of the Dutch type (HCHWA-D), an autosomal dominant form of cerebral amyloid angiopathy (CAA), is characterized by extensive amyloid deposition in the small leptomeningeal arteries and cortical arterioles, which lead to an early death of those afflicted in their fifth or sixth decade. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cellular senescence is a homeostatic biological process characterized by a permanent state of cell cycle arrest that can contribute to the decline of the regenerative potential and function of tissues. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Protease nexin-II (PN-II) [amyloid beta-protein precursor (APP)] and the amyloid beta-protein are major constituents of neuritic plaques and cerebrovascular deposits in individuals with Alzheimer's disease and Down syndrome. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 8,460 studies in this tag that have a study page, 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.
- Assessment of cerebrospinal fluid (CSF) beta-amyloid (1-42), phosphorylated tau (ptau-181) and total Tau protein in patients with Alzheimer's disease (AD) and other dementia at Siriraj Hospital, Thailand
- The roles of apolipoprotein E ε4 on neuropathology and neuroinflammation in patients with Alzheimer's disease
- Multifaceted role of nitric oxide in vascular dementia
- Systemic inflammatory regulators and risk of Alzheimer's disease: a bidirectional Mendelian-randomization study
- PIN1-p53 bifurcation dictates opposite cell fate decisions in Alzheimer’s disease and glioblastoma via distinct energy landscape topologies
- Comparative lipidomic analysis of mouse and human brain with Alzheimer disease
- Proteomic analysis of protein homeostasis and aggregation
- Alborixin clears amyloid-β by inducing autophagy through PTEN-mediated inhibition of the AKT pathway
- The role of plasma inflammatory markers in late-life depression and conversion to dementia: a 3-year follow-up study
- Apolipoprotein E: high-avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial Alzheimer 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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events