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Research

30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1–25 of 29 studies by Li X · tagged Brain Biology (page 1 of 2) · 30,580 in the whole library · How the 0–100 score works

Download bibliography of these 29 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

Other authors

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

Institutions

From OpenAlex; 16,054 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.

S-nitrosylation of parkin regulates ubiquitination and compromises parkin's protective function

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Science (New York, N.Y.) 2004-04-22

Parkin is an E3 ubiquitin ligase involved in the ubiquitination of proteins that are important in the survival of dopamine neurons in Parkinson's disease (PD). 4 key findings →

Evidence: low

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

Apolipoprotein E Is a Ligand for Triggering Receptor Expressed on Myeloid Cells 2 (TREM2)

✓ Peer-reviewed alzhub usefulness score 54 out of 100. The Journal of biological chemistry 2015-09-15

Several heterozygous missense mutations in the triggering receptor expressed on myeloid cells 2 (TREM2) have recently been linked to risk for a number of neurological disorders including Alzheimer disease (AD), Parkinson disease, and frontotemporal dementia. 1 key finding →

Evidence: low

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

A tetravalent TREM2 agonistic antibody reduced amyloid pathology in a mouse model of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Science translational medicine 2022-09-07

Triggering receptor expressed on myeloid cells 2 (TREM2) plays crucial roles in Alzheimer's disease (AD) by regulating microglia migration toward, and phagocytosis of oligomeric amyloid-β (oAβ) and amyloid plaques. 4 key findings →

Evidence: low

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

Multi-omic comparison of Alzheimer's variants in human ESC-derived microglia reveals convergence at APOE

✓ Peer-reviewed alzhub usefulness score 50 out of 100. The Journal of experimental medicine 2020-12-01

Variations in many genes linked to sporadic Alzheimer's disease (AD) show abundant expression in microglia, but relationships among these genes remain largely elusive. 4 key findings →

Evidence: low

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

Colocalization of cerebral iron with Amyloid beta in Mild Cognitive Impairment

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Scientific reports 2016-10-17

Quantitative Susceptibility Mapping (QSM) MRI at 7 Tesla and 11-Carbon Pittsburgh-Compound-B PET were used for investigating the relationship between brain iron and Amyloid beta (Aβ) plaque-load in a context of increased risk for Alzheimer's disease (AD), as reflected by the Apolipoprotein E ε4 (APOE-e4) allele and mild cognitive impairment (MCI) in elderly subjects. 4 key findings →

Evidence: low

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

Tau seeds from Alzheimer's disease brains trigger tau spread in macaques while oligomeric-Aβ mediates pathology maturation

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2023-12-26

Oligomeric-Aβ mediates the maturation of tau pathology and its neuronal toxicity in macaques but not its initial spreading. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

New Insights into Neuroinflammation Involved in Pathogenic Mechanism of Alzheimer's Disease and Its Potential for Therapeutic Intervention

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Cells 2022-06-14

Alzheimer's disease (AD) is the most common form of dementia, affecting more than 50 million people worldwide with an estimated increase to 139 million people by 2050. 4 key findings →

Evidence: low

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

TREM2 protects against cerebral ischemia/reperfusion injury

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Molecular brain 2017-06-07

Although post-ischemic inflammation induced by the innate immune response is considered an essential step in the progression of cerebral ischemia injury, the role of triggering receptor expressed on myeloid cells 2 (TREM2) in the pathogenesis of ischemic stroke remains to be elucidated. 4 key findings →

Evidence: low

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

Ex vivo expanded human regulatory T cells modify neuroinflammation in a preclinical model of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Acta neuropathologica communications 2022-09-30

Regulatory T cells (Tregs) play a neuroprotective role by suppressing microglia and macrophage-mediated inflammation and modulating adaptive immune reactions. 4 key findings →

Evidence: low

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

Identification of the novel activity-driven interaction between synaptotagmin 1 and presenilin 1 links calcium, synapse, and amyloid beta

✓ Peer-reviewed alzhub usefulness score 40 out of 100. BMC biology 2016-03-31

Our findings identify Syt1 as a novel Ca(2+)-sensitive PS1 modulator that could regulate synaptic Aβ, opening avenues for novel and selective synapse targeting therapeutic strategies. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Chronic exposure of alcohol triggers microglia-mediated synaptic elimination inducing cognitive impairment

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Experimental neurology 2022-04-01

Our data suggests that TREM2 is associated with synaptic plasticity impairment and memory deficits, indicating microglia-mediated synaptic pruning might be the underlying mechanism involved in synapse loss and memory impairment induced by long-term alcohol intake. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Upregulation of TREM2 Ameliorates Neuroinflammatory Responses and Improves Cognitive Deficits Triggered by Surgical Trauma in Appswe/PS1dE9 Mice

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 2018-04-18

The downregulation of TREM2 exacerbated surgery-induced cognitive deficits and exaggerated neuroinflammatory responses in this rodent model. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Activation of FAK/Rac1/Cdc42-GTPase signaling ameliorates impaired microglial migration response to Aβ42 in triggering receptor expressed on myeloid cells 2 loss-of-function murine models

✓ Peer-reviewed alzhub usefulness score 38 out of 100. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2020-07-01

Mutation of Triggering receptor expressed on myeloid cells 2 (TREM2) impairs the response of microglia to amyloid-β (Aβ) pathology in Alzheimer's disease (AD), although the mechanism governing TREM2-regulated microglia recruitment to Aβ plaques remains unresolved. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

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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