Alzheimer's disease (AD) lesions are characterized by the presence of numerous inflammatory proteins.
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Research
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
1. Of the neurodegenerative diseases that cause dementia, Alzheimer's disease (AD) is the most common. 2 key findings →
Design: longitudinal study Evidence: moderate
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52/100
Alzheimer disease (AD) and chronic traumatic encephalopathy (CTE) involve the abnormal accumulation in the brain of filaments composed of both three-repeat (3R) and four-repeat (4R) (3R/4R) tau isoforms. 1 key finding →
Participants: 16 Evidence: low
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Primary age-related tauopathy (PART) is a form of Alzheimer-type neurofibrillary degeneration occurring in the absence of amyloid-beta (Aβ) plaques. 3 key findings →
Participants: 174 Evidence: low
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Argyrophilic grain disease (AGD) is a frequent late-onset, 4-repeat tauopathy reported in Caucasians with high educational attainment. 2 key findings →
Participants: 983 Evidence: moderate
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52/100
Primary age-related tauopathy (PART) is a neurodegenerative entity defined as Alzheimer-type neurofibrillary degeneration primarily affecting the medial temporal lobe with minimal to absent amyloid-β (Aβ) plaque deposition. 3 key findings →
Participants: 914 Evidence: moderate
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Dogs develop cognitive decline and a progressive accumulation of oxidative damage. 3 key findings →
Design: longitudinal study Evidence: moderate
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One of the hallmarks of Alzheimer's disease is abnormal deposition of tau proteins in the brain. 3 key findings →
Design: cross-sectional Evidence: moderate
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The hippocampal formation plays an important role in cognition, spatial navigation, learning, and memory. 5 key findings →
Design: longitudinal study Evidence: moderate
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Plasma biomarkers related to amyloid, tau, and neurodegeneration (ATN) show great promise for identifying these pathological features of Alzheimer's Disease (AD) as shown by recent clinical studies and selected autopsy studies. 2 key findings →
Evidence: low
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Studies on markers of inflammation in subjects with mild cognitive impairment or AD dementia provided inconsistent results. 5 key findings →
Design: cross-sectional Participants: 48 Evidence: low
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We examined whether plasma p-tau181 and p-tau217 are specific biomarkers of pathologically confirmed Alzheimer's disease (AD). 5 key findings →
Evidence: low
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Corticobasal degeneration (CBD) is a neurodegenerative tauopathy-a class of disorders in which the tau protein forms insoluble inclusions in the brain-that is characterized by motor and cognitive disturbances 1-3 . 5 key findings →
Evidence: low
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The role of DNA cytosine methylation, an epigenetic regulator of chromatin structure and function, during normal and pathological brain development and aging remains unclear. 1 key finding →
Participants: 125 Evidence: moderate
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52/100
More specifically, 18F-AV-1451 binding was significantly increased in patients with Alzheimer's disease, relative to patients with progressive supranuclear palsy and with control subjects, in the hippocampus and in occipital, parietal, temporal, and frontal cortices (t's > 2.2, P's < 0.04). 4 key findings →
Participants: 15 Evidence: low
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Tau vulnerability in women is not just limited to the medial temporal lobe and significantly contributed to greater risk of faster cognitive decline. 2 key findings →
Participants: 55 Evidence: moderate
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52/100
We found significant group-wise differences in 11C-PK-11195 binding between each patient group and controls in frontotemporal regions, in both a regions-of-interest analysis and in the comparison of principal spatial components of binding. 18F-AV-1451 binding was increased in semantic variant primary progressive aphasia compared to controls in the temporal regions, and both semantic variant primary progressive aphasia and behavioural variant frontotemporal dementia differed from controls in the expression of principal spatial components of binding, across temporal and frontotemporal cortex, respectively. 2 key findings →
Participants: 31 Evidence: low
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We provide the first evidence for the capability of a high-resolution positron emission tomographic (PET) imaging system in quantitatively mapping amyloid accumulation in living amyloid precursor protein transgenic (Tg) mice. 3 key findings →
Design: longitudinal study Evidence: moderate
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CAARS has the potential to predict CAA severity; however, its clinical utility should be evaluated in follow-up studies. 3 key findings →
Evidence: moderate
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Inflammation is a physiological process that repairs tissues in response to endogenous or exogenous aggressions. 2 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The Religious Orders Study is a longitudinal clinical-pathologic cohort study of aging and Alzheimer's disease (AD). 1 key finding →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
52/100
Plasma A+/T + individuals showed the highest levels of astrocyte reactivity, Aβ plaque, tau tangle, and axonal degeneration, and the lowest hippocampal volume and temporal-metaROI cortical thickness. 5 key findings →
Participants: 470 Evidence: low
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CRM-adjusted Aβ42 calibrator concentrations were calculated using the regression equation Y (CRM-adjusted) = 0.89X (calibrators) + 32.6. 5 key findings →
Participants: 766 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma β-synuclein levels were higher in preclinical AD and even higher in MCI and AD dementia. 5 key findings →
Participants: 48 Evidence: low
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β-blockers that easily cross the blood-brain barrier (BBB) seem to diminish the risk of Alzheimer's disease (AD), hypothetically facilitating waste clearance. 3 key findings →
Participants: 216 Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 6,970 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.
- Reelin protects against amyloid β toxicity in vivo
- Energy Thresholds in Brain Mitochondria
- Trem2R47H and reduced TREM2 expression both mimic human Alzheimer's disease signatures in mice
- Frequency of LATE neuropathologic change across the spectrum of Alzheimer's disease neuropathology: combined data from 13 community-based or population-based autopsy cohorts
- Defects in lysosomal function and lipid metabolism in human microglia harboring a TREM2 loss of function mutation
- X-34, a fluorescent derivative of Congo red: a novel histochemical stain for Alzheimer's disease pathology
- Identification and therapeutic modulation of a pro-inflammatory subset of disease-associated-microglia in Alzheimer's disease
- Inflammation in ALS/FTD pathogenesis
- Exploring the Pathogenesis of Alzheimer Disease in Basal Forebrain Cholinergic Neurons and Converging Insights from Alternative Hypothesis
- FGF21 Attenuates High-Fat Diet-Induced Cognitive Impairment via Metabolic Regulation and Anti-inflammation of Obese Mice
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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →