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Research

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

Find studies

Showing 51–75 of 149 studies in Molecular psychiatry (page 3 of 6) · 30,580 in the whole library · How the 0–100 score works

Download bibliography of these 149 studies, in this order: BibTeX (.bib) · RIS (.ris)

This list as a page: Molecular Psychiatry in the library →

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; 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.

Individual regional associations between Aβ-, tau- and neurodegeneration (ATN) with microglial activation in patients with primary and secondary tauopathies

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Molecular psychiatry 2023-07-26

β-amyloid (Aβ) and tau aggregation as well as neuronal injury and atrophy (ATN) are the major hallmarks of Alzheimer's disease (AD), and biomarkers for these hallmarks have been linked to neuroinflammation. 2 key findings →

Participants: 55 Evidence: moderate

Full summary, score breakdown and related studies → Original source

Florbetapir F 18 amyloid PET and 36-month cognitive decline: a prospective multicenter study

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Molecular psychiatry 2014-03-11

This study was designed to evaluate whether subjects with amyloid beta (Aβ) pathology, detected using florbetapir positron emission tomorgraphy (PET), demonstrated greater cognitive decline than subjects without Aβ pathology. 4 key findings →

Evidence: low

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

APOE and BCHE as modulators of cerebral amyloid deposition: a florbetapir PET genome-wide association study

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Molecular psychiatry 2013-02-19

Deposition of amyloid-β (Aβ) in the cerebral cortex is thought to be a pivotal event in Alzheimer's disease (AD) pathogenesis with a significant genetic contribution. 3 key findings →

Participants: 555 Evidence: low

Full summary, score breakdown and related studies → Original source

Tau pathology is associated with synaptic density and longitudinal synaptic loss in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Molecular psychiatry 2024-04-08

The associations of synaptic loss with amyloid-β (Aβ) and tau pathology measured by positron emission tomography (PET) and plasma analysis in Alzheimer's disease (AD) patients are unknown. 4 key findings →

Design: cross-sectional Evidence: moderate

Full summary, score breakdown and related studies → Original source

Age, sex and APOE-ε4 modify the balance between soluble and fibrillar β-amyloid in non-demented individuals: topographical patterns across two independent cohorts

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Molecular psychiatry 2022-03-02

Amyloid (Aβ) pathology is the earliest detectable pathophysiological event along the Alzheimer's continuum, which can be measured both in the cerebrospinal fluid (CSF) and by Positron Emission Tomography (PET). 2 key findings →

Participants: 320 Evidence: low

Full summary, score breakdown and related studies → Original source

Tau PET positivity predicts clinically relevant cognitive decline driven by Alzheimer's disease compared to comorbid cases; proof of concept in the ADNI study

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Molecular psychiatry 2024-08-23

β-amyloid (Aβ) pathology is not always coupled with Alzheimer's disease (AD) relevant cognitive decline. 3 key findings →

Participants: 70 Evidence: low

Full summary, score breakdown and related studies → Original source

Examination of the current top candidate genes for AD in a genome-wide association study

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Molecular psychiatry 2009-01-06

With the advent of technologies that allow simultaneous genotyping of thousands of single-nucleotide polymorphisms (SNPs) across the genome, the genetic contributions to complex diseases can be explored at an unprecedented detail. 5 key findings →

Design: case-control study Evidence: moderate

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

Patient-specific Alzheimer-like pathology in trisomy 21 cerebral organoids reveals BACE2 as a gene dose-sensitive AD suppressor in human brain

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Molecular psychiatry 2020-07-10

A population of more than six million people worldwide at high risk of Alzheimer's disease (AD) are those with Down Syndrome (DS, caused by trisomy 21 (T21)), 70% of whom develop dementia during lifetime, caused by an extra copy of β-amyloid-(Aβ)-precursor-protein gene. 1 key finding →

Evidence: low

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

Integrative brain transcriptome analysis links complement component 4 and HSPA2 to the APOE ε2 protective effect in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Molecular psychiatry 2021-09-03

Mechanisms underlying the protective effect of apolipoprotein E (APOE) ε2 against Alzheimer disease (AD) are not well understood. 4 key findings →

Participants: 982 Evidence: low

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

Higher plasma soluble TREM2 correlates with reduced cerebral tau accumulation in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Molecular psychiatry 2025-04-01

Loss-of-function mutation of triggering receptor expressed on myeloid cell 2 (TREM2) is associated with increased risks for Alzheimer's disease (AD). 3 key findings →

Participants: 129 Evidence: low

Full summary, score breakdown and related studies → Original source

Whole-genome sequencing suggests a chemokine gene cluster that modifies age at onset in familial Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Molecular psychiatry 2015-09-01

We have sequenced the complete genomes of 72 individuals affected with early-onset familial Alzheimer's disease caused by an autosomal dominant, highly penetrant mutation in the presenilin-1 (PSEN1) gene, and performed genome-wide association testing to identify variants that modify age at onset (AAO) of Alzheimer's disease. 4 key findings →

Participants: 72 Evidence: moderate

Full summary, score breakdown and related studies → Original source

Convergent functional genomics of schizophrenia: from comprehensive understanding to genetic risk prediction

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Molecular psychiatry 2012-05-15

We have used a translational convergent functional genomics (CFG) approach to identify and prioritize genes involved in schizophrenia, by gene-level integration of genome-wide association study data with other genetic and gene expression studies in humans and animal models. 3 key findings →

Evidence: low

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

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

Shared genetic aetiology between cognitive functions and physical and mental health in UK Biobank (N=112 151) and 24 GWAS consortia

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Molecular psychiatry 2016-01-26

Causes of the well-documented association between low levels of cognitive functioning and many adverse neuropsychiatric outcomes, poorer physical health and earlier death remain unknown. 4 key findings →

Participants: 112 Evidence: low

Full summary, score breakdown and related studies → Original source

Sex differences in plasma p-tau181 associations with Alzheimer's disease biomarkers, cognitive decline, and clinical progression

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Molecular psychiatry 2022-06-29

Studies have shown that women on the Alzheimer's disease (AD) continuum have more pathological tau in the brain and cerebrospinal fluid (CSF), than men. 4 key findings →

Evidence: low

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

Use of an Alzheimer's disease polygenic risk score to identify mild cognitive impairment in adults in their 50s

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Molecular psychiatry 2018-02-27

Early identification of younger, non-demented adults at elevated risk for Alzheimer's disease (AD) is crucial because the pathological process begins decades before dementia onset. 5 key findings →

Evidence: low

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

Plasma biosignature and brain pathology related to persistent cognitive impairment in late-life depression

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Molecular psychiatry 2014-08-05

Cognitive impairment is highly prevalent among individuals with late-life depression (LLD) and tends to persist even after successful treatment. 5 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
  • 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