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Research

28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1,626–1,650 of 7,821 studies · tagged Brain Biology (page 66 of 313) · 28,980 in the whole library · How the 0–100 score works

Download bibliography of the first 500 of these studies, in this order: BibTeX (.bib) · RIS (.ris)

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

Subjects

Authors

Names as each record prints them; the same person can appear under two spellings.

Institutions

From OpenAlex; 14,457 studies have no institution on record and are not counted here.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

Gain and loss of function of ALS-related mutations of TARDBP (TDP-43) cause motor deficits in vivo

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Human molecular genetics 2009-12-03

TDP-43 has been found in inclusion bodies of multiple neurological disorders, including amyotrophic lateral sclerosis, frontotemporal dementia, Parkinson's disease and Alzheimer's disease. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Alzheimer disease with amygdala Lewy bodies: a distinct form of alpha-synucleinopathy

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Journal of neuropathology and experimental neurology 2006-07-01

Lewy bodies (LBs) are alpha-synuclein-immunoreactive neuronal inclusions with a predilection for specific cortical and subcortical regions, including the amygdala. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Colocalization of tau and alpha-synuclein epitopes in Lewy bodies

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Journal of neuropathology and experimental neurology 2003-04-01

The major protein constituent of Lewy bodies (LBs), the pathological hallmark of Parkinson disease and dementia with Lewy bodies, is considered to be alpha-synuclein, but other proteins, in particular the microtubule-associated protein tau, have been implicated in the pathogenesis of LBs. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Cerebrovascular dysfunction and microcirculation rarefaction precede white matter lesions in a mouse genetic model of cerebral ischemic small vessel disease

✓ Peer-reviewed alzhub usefulness score 50 out of 100. The Journal of clinical investigation 2010-01-11

Cerebral ischemic small vessel disease (SVD) is the leading cause of vascular dementia and a major contributor to stroke in humans. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Oxidative Stress, Amyloid-β Peptide, and Altered Key Molecular Pathways in the Pathogenesis and Progression of Alzheimer's Disease

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Journal of Alzheimer's disease : JAD 2018-01-01

Oxidative stress is implicated in the pathogenesis and progression of Alzheimer's disease (AD) and its earlier stage, amnestic mild cognitive impairment (aMCI). 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Alteration of mTOR signaling occurs early in the progression of Alzheimer disease (AD): analysis of brain from subjects with pre-clinical AD, amnestic mild cognitive impairment and late-stage AD

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Journal of neurochemistry 2015-02-26

The clinical symptoms of Alzheimer disease (AD) include a gradual memory loss and subsequent dementia, and neuropathological deposition of senile plaques and neurofibrillary tangles. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Microglial activation by Alzheimer amyloid precursor protein and modulation by apolipoprotein E

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Nature 1997-08-01

A role for beta-amyloid precursor protein (beta-APP) in the development of Alzheimer's disease has been indicated by genetics, and many conditions in which beta-APP is raised have been associated with an increased risk of Alzheimer's disease or an Alzheimer's-like pathology. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

A disintegrin-metalloproteinase prevents amyloid plaque formation and hippocampal defects in an Alzheimer disease mouse model

✓ Peer-reviewed alzhub usefulness score 50 out of 100. The Journal of clinical investigation 2004-05-01

Alzheimer disease (AD) is characterized by excessive deposition of amyloid beta-peptides (A beta peptides) in the brain. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Generation of beta-amyloid in the secretory pathway in neuronal and nonneuronal cells

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1993-03-01

The cellular mechanism underlying the generation of beta-amyloid in Alzheimer disease and its relationship to the normal metabolism of the amyloid precursor protein are unknown. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

The presenilin 2 mutation (N141I) linked to familial Alzheimer disease (Volga German families) increases the secretion of amyloid beta protein ending at the 42nd (or 43rd) residue

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1997-03-01

To gain insights into the significance of presenilins (PS) in the pathogenetic mechanisms of early-onset familial Alzheimer disease (FAD), we expressed cDNAs for wild-type PS2 and PS2 with the Volga German (N141I) mutation in cultured cells and then examined the metabolism of the transfected proteins and their effect on the C-terminal properties of secreted amyloid beta protein (A beta). 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Amyloid beta-protein is degraded by cellular angiotensin-converting enzyme (ACE) and elevated by an ACE inhibitor

✓ Peer-reviewed alzhub usefulness score 50 out of 100. The Journal of biological chemistry 2005-09-09

Human genetic data have associated angiotensin-converting enzyme (ACE) with Alzheimer disease (AD), and purified ACE has been reported to cleave synthetic amyloid beta-protein (Abeta) in vitro. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Oxidative modification and down-regulation of Pin1 in Alzheimer's disease hippocampus: A redox proteomics analysis

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Neurobiology of aging 2005-06-13

Alzheimer disease (AD) is characterized neuropathologically by intracellular neurofibrillary tangles (NFT) and of extracellular senile plaques (SP), the central core of which is amyloid beta-peptide (Abeta) derived from amyloid precursor protein (APP), a transmembrane protein. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Tumor necrosis factor-α synthesis inhibitor 3,6'-dithiothalidomide attenuates markers of inflammation, Alzheimer pathology and behavioral deficits in animal models of neuroinflammation and Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Journal of neuroinflammation 2012-05-29

Neuroinflammation is associated with virtually all major neurodegenerative disorders, including Alzheimer's disease (AD). 4 key findings →

Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

High striatal amyloid beta-peptide deposition across different autosomal Alzheimer disease mutation types

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Archives of neurology 2009-12-01

Mutations in the amyloid precursor protein (APP), presenilin 1 (PSEN1), and presenilin 2 (PSEN2) genes lead to increased Abeta levels before symptoms arise. 4 key findings →

Participants: 30 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Aβ-induced acceleration of Alzheimer-related τ-pathology spreading and its association with prion protein

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Acta neuropathologica 2019-08-14

Extracellular deposition of amyloid β-protein (Aβ) in amyloid plaques and intracellular accumulation of abnormally phosphorylated τ-protein (p-τ) in neurofibrillary tangles (NFTs) represent pathological hallmark lesions of Alzheimer's disease (AD). 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

TREMs in the immune system and beyond

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Nature reviews. Immunology 2003-06-01

Triggering receptors expressed by myeloid cells (TREMs) belong to a rapidly expanding family of receptors that include activating and inhibitory isoforms encoded by a gene cluster linked to the MHC. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Trem2 Deletion Reduces Late-Stage Amyloid Plaque Accumulation, Elevates the Aβ42:Aβ40 Ratio, and Exacerbates Axonal Dystrophy and Dendritic Spine Loss in the PS2APP Alzheimer's Mouse Model

✓ Peer-reviewed alzhub usefulness score 50 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2020-01-24

TREM2 is an Alzheimer's disease (AD) risk gene expressed in microglia. 4 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.

↑ Change the filters

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 →

Newest studies, as a dated timeline →    Atom feed