Oxidative damage is a major feature in the pathophysiology of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Abeta is the major component of amyloid plaques characterizing Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
36/100
Amyloid-β proteins (Aβ) of 42 (Aβ42) and 40 aa (Aβ40) accumulate as senile plaques (SP) and cerebrovascular amyloid protein deposits that are defining diagnostic features of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Humans have evolved much longer lifespans than the great apes, which rarely exceed 50 years. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Spherical Abeta-containing elements, which are typically organized as concentric ring-like structures, are common substructural components of drusen. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Myeloperoxidase (MPO) is a myeloid-specific enzyme that generates hypochlorous acid and other reactive oxygen species. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The epsilon4 allele of apolipoprotein E (apoE) is a risk factor for Alzheimer's disease (AD), perhaps through effects on amyloid-beta (Abeta) metabolism. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein (apo) E, a polymorphic protein with three isoforms (apoE2, apoE3, and apoE4), is essential for lipid homeostasis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common cause of dementia, affecting 35 million people today. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline and neuropathological changes, including the deposition of amyloid beta (Abeta) in senile plaques. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Addition of the beta-hydroxy-beta-methylglutaryl-CoA (HmG-CoA) reductase inhibitor lovastatin to human HEK cells transfected with the amyloid precursor protein (APP) reduces intracellular cholesterol/protein ratios by 50%, and markedly inhibits beta-secretase cleavage of newly-synthesized APP. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The present study examines N-myc and c-myc protein expression with Western blotting and single and double-labeling immunohistochemistry in the hippocampus in Alzheimer disease (AD), the striatum in Huntington disease (HD) and the substantia nigra in Parkinson disease (PD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer disease has been well associated with mitochondrial dysfunctions. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Brain spectrin is a major membrane skeleton protein that participates in cellular transport, cell morphogenesis, neurotransmitter release and growth cone adhesion. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
An important worldwide health problem as the result of current lifestyle is metabolic syndrome (MS). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The progressive nature of neurodegeneration suggests an age-dependent process that ultimately leads to synaptic failure and neuronal damage in cortical areas of the brain critical for memory and higher mental functions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Prenatal exposure to low doses of LPS caused AD-related features including behavioral and neuropathological changes from midlife to senectitude. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These findings suggest that neurotrophic impairment during early development can be one of the etiopathogenic factors of AD and that the neurotrophic peptide mimetic is a potential early prevention strategy for this disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebral amyloid angiopathy (CAA) is caused by the cerebrovascular deposition of Alzheimer amyloid beta protein (Abeta) and shows an increased incidence in carriers of the apolipoprotein E (APOE) epsilon4 genotype. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
When evaluating the 'bleeding load' with 7.0-T T₂*-weighted MRI in post-mortem brain sections of patients with dementia and vascular risk factors, only quantification of small cerebral bleeds in the cortico-subcortical regions is reliable. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer's disease (AD) is the most common cause of dementia in the elderly population. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
This study adds further arguments for a cognitive impairment in MND/ALS. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Down syndrome individuals develop abnormalities of most organs, including all the pathological and neurochemical features of Alzheimer's disease, by the early age of 30 yr. Here, we report the isolation and characterization of BACE2, a gene mapping on human chromosome 21q22.3, which is highly similar to a transmembrane aspartyl protease, BACE (for beta-site APP-cleaving enzyme), which is able to catalyze the beta-secretase cleavage of Alzheimer's amyloid precursor protein (APP). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
In Alzheimer disease brains, the amyloid plaques are closely associated with a locally induced, nonimmune-mediated, chronic inflammatory response without any apparent influx of leukocytes from the blood. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Oxidative stress is a phenomenon associated with imbalance between production of free radicals and reactive metabolites (e.g. superoxide and hydrogen peroxide) and the antioxidant defences. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
From across this tag
10 of the 7,799 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.
- Sustained hippocampal IL-1 beta overexpression mediates chronic neuroinflammation and ameliorates Alzheimer plaque pathology
- Invited review: Estrogens effects on the brain: multiple sites and molecular mechanisms
- The role of DYRK1A in neurodegenerative diseases
- A genome-wide association study in human lymphoblastoid cells supports safety of mitochondrial complex I inhibitor
- 18F-AV-1451 positron emission tomography in neuropathological substrates of corticobasal syndrome
- APOE genotype alters glial activation and loss of synaptic markers in mice
- Common human genetic variants of APOE impact murine COVID-19 mortality
- The pattern of acquisition of plaques and tangles in the brains of patients under 50 years of age with Down's syndrome
- Aβ positive, tau biomarker negative cognitive impairment is associated with significant non‐Alzheimer's disease neuropathologies
- Amyloid precursor protein processing and A beta42 deposition in a transgenic mouse model of 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 28,980 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 28,980 records, built mostly from automated pulls of Europe PMC (62.8% of the library) and OpenAlex (17.6%), 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.
1,038 records (3.6% of the library) are not peer-reviewed — 966 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 →