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Research

31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 26–50 of 58 studies with an author at Inserm (FR) (page 2 of 3) · 31,380 in the whole library · How the 0–100 score works

Download bibliography of these 58 studies, in this order: BibTeX (.bib) · RIS (.ris)

Showing 58 studies tagged precursor — clear

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.

Other institutions

From OpenAlex; 16,851 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.

The effect of increased genetic risk for Alzheimer's disease on hippocampal and amygdala volume

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Neurobiology of aging 2016-01-11

Reduction in hippocampal and amygdala volume measured via structural magnetic resonance imaging is an early marker of Alzheimer's disease (AD). 4 key findings →

Design: case-control study Evidence: moderate

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

Beta-amyloid burden in the temporal neocortex is related to hippocampal atrophy in elderly subjects without dementia

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Neurology 2010-01-01

The strong correlation between hippocampal atrophy and beta-amyloid (Abeta) burden in the Pittsburgh compound B-positive healthy control group suggests that Abeta deposition in the inferior temporal neocortex is related to hippocampal synaptic and neuronal degeneration. 3 key findings →

Participants: 32 Evidence: low

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

Neutrophil hyperactivation correlates with Alzheimer's disease progression

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Annals of neurology 2018-02-01

Our results indicate that the inflammatory properties of circulating neutrophils shift as the percentage of aged neutrophils expands in patients with AD-changes that may play an instrumental role in establishing systemic chronic inflammation. 3 key findings →

Participants: 42 Evidence: low

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

Regulatory T cells delay disease progression in Alzheimer-like pathology

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Brain : a journal of neurology 2016-02-01

Recent studies highlight the implication of innate and adaptive immunity in the pathophysiology of Alzheimer's disease, and foster immunotherapy as a promising strategy for its treatment. 4 key findings →

Evidence: low

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

Novel Alzheimer risk genes determine the microglia response to amyloid-β but not to TAU pathology

✓ Peer-reviewed alzhub usefulness score 52 out of 100. EMBO molecular medicine 2020-01-17

Polygenic risk scores have identified that genetic variants without genome-wide significance still add to the genetic risk of developing Alzheimer's disease (AD). 2 key findings →

Evidence: low

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

Resting metabolic connectivity in prodromal Alzheimer's disease. A European Alzheimer Disease Consortium (EADC) project

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Neurobiology of aging 2012-02-23

We explored resting-state metabolic connectivity in prodromal Alzheimer's disease (pAD) patients and in healthy controls (CTR), through a voxel-wise interregional correlation analysis of 18F-fluorodeoxyglucose (FDG)-positron emission tomography (PET) by means of statistical parametric mapping. 1 key finding →

Participants: 36 Evidence: low

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

High frequency of potentially pathogenic SORL1 mutations in autosomal dominant early-onset Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Molecular psychiatry 2012-04-03

Performing exome sequencing in 14 autosomal dominant early-onset Alzheimer disease (ADEOAD) index cases without mutation on known genes (amyloid precursor protein (APP), presenilin1 (PSEN1) and presenilin2 (PSEN2)), we found that in five patients, the SORL1 gene harbored unknown nonsense (n=1) or missense (n=4) mutations. 4 key findings →

Evidence: low

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

Contribution to Alzheimer's disease risk of rare variants in TREM2, SORL1, and ABCA7 in 1779 cases and 1273 controls

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Neurobiology of aging 2017-07-14

We performed whole-exome and whole-genome sequencing in 927 late-onset Alzheimer disease (LOAD) cases, 852 early-onset AD (EOAD) cases, and 1273 controls from France. 4 key findings →

Evidence: low

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

Viral gene transfer of APPsα rescues synaptic failure in an Alzheimer's disease mouse model

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Acta neuropathologica 2015-11-04

Alzheimer's disease (AD) is characterized by synaptic failure, dendritic and axonal atrophy, neuronal death and progressive loss of cognitive functions. 4 key findings →

Evidence: low

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

APOE-stratified genome-wide association analyses provide insights into the genetic etiology of Alzheimers's disease

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Nature genetics 2026-09-14

Among the more than 90 identified genetic risk loci for late-onset Alzheimer's disease (AD) and related dementias, the apolipoprotein E (APOE) gene ɛ2/ɛ3/ɛ4 polymorphisms remain the longstanding benchmark for genetic disease risk with a consistently large effect across studies 1-10 . 5 key findings →

Design: case-control Evidence: high

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

Accelerated cortical atrophy in cognitively normal elderly with high β-amyloid deposition

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Neurology 2012-02-01

Our findings show that the presence of Aβ in the brain, known to occur in about one-third of asymptomatic elderly individuals, is actually a pathologic state associated with accelerated atrophy. 4 key findings →

Evidence: low

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

Influence of microglial activation on neuronal function in Alzheimer's and Parkinson's disease dementia

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2014-09-16

Alzheimer's disease (AD) and Parkinson's disease (PD) are the two common neurodegenerative diseases characterized by progressive neuronal dysfunction in the presence of pathological microglial activation. 4 key findings →

Evidence: low

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

Truncated beta-amyloid peptide species in pre-clinical Alzheimer's disease as new targets for the vaccination approach

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Journal of neurochemistry 2003-06-01

Vaccination against human beta-amyloid peptide (A beta) has been shown to remove the amyloid burden produced in transgenic mice overexpressing the mutated human amyloid precursor protein (APP) gene. 4 key findings →

Evidence: low

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

De novo deleterious genetic variations target a biological network centered on Aβ peptide in early-onset Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Molecular psychiatry 2015-07-21

We hypothesized that de novo variants (DNV) might participate in the genetic determinism of sporadic early-onset Alzheimer disease (EOAD, onset before 65 years). 4 key findings →

Evidence: low

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

The French series of autosomal dominant early onset Alzheimer's disease cases: mutation spectrum and cerebrospinal fluid biomarkers

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Journal of Alzheimer's disease : JAD 2012-01-01

We describe 56 novel autosomal dominant early-onset Alzheimer disease (ADEOAD) families with PSEN1, PSEN2, and AβPP mutations or duplications, raising the total of families with mutations on known genes to 111 (74 PSEN1, 8 PSEN2, 16 AβPP, and 13 AβPP duplications) in the French series. 4 key findings →

Evidence: low

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

Whole exome sequencing study identifies novel rare and common Alzheimer's-Associated variants involved in immune response and transcriptional regulation

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Molecular psychiatry 2018-08-14

The Alzheimer's Disease Sequencing Project (ADSP) undertook whole exome sequencing in 5,740 late-onset Alzheimer disease (AD) cases and 5,096 cognitively normal controls primarily of European ancestry (EA), among whom 218 cases and 177 controls were Caribbean Hispanic (CH). 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

ApoE immunoreactivity and microglial cells in Alzheimer's disease brain

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Neuroscience letters 1995-07-01

The spatial relationship of apolipoprotein E (apoE)-like immunoreactivity (IR) to amyloid beta-peptide (A beta), astrocytes and microglial cells in the brain of Alzheimer's disease was studied by double immunolabelling. 1 key finding →

Evidence: low

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

Metabolic networks underlying cognitive reserve in prodromal Alzheimer disease: a European Alzheimer disease consortium project

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Journal of nuclear medicine : official publication, Society of Nuclear Medicine 2013-04-16

The clusters of significant depression and compensation were further used as volumetric regions of interest (ROIs) in a brain interregional correlation analysis in each prodromal AD subgroup to explore metabolic connectivity. 3 key findings →

Evidence: low

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

Amyloid Precursor Protein (APP) Metabolites APP Intracellular Fragment (AICD), Aβ42, and Tau in Nuclear Roles

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 2015-08-21

Amyloid precursor protein (APP) metabolites (amyloid-β (Aβ) peptides) and Tau are the main components of senile plaques and neurofibrillary tangles, the two histopathological hallmarks of Alzheimer disease. 3 key findings →

Evidence: low

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

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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
  • Randomized / 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
  • Multicenter 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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.

1,048 records (3.3% of the library) are not peer-reviewed — 973 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