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Research

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

Find studies

Showing 51–75 of 76 studies with an author at Columbia University (US) (page 3 of 4) · 31,380 in the whole library · How the 0–100 score works

Download bibliography of these 76 studies, in this order: BibTeX (.bib) · RIS (.ris)

Showing 76 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.

Location of pathogenic variants in PSEN1 impacts progression of cognitive, clinical, and neurodegenerative measures in autosomal-dominant Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Aging cell 2023-06-08

Although pathogenic variants in PSEN1 leading to autosomal-dominant Alzheimer disease (ADAD) are highly penetrant, substantial interindividual variability in the rates of cognitive decline and biomarker change are observed in ADAD. 3 key findings →

Design: cross-sectional Evidence: moderate

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

Increased localization of APP-C99 in mitochondria-associated ER membranes causes mitochondrial dysfunction in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 51 out of 100. The EMBO journal 2017-10-10

In the amyloidogenic pathway associated with Alzheimer disease (AD), the amyloid precursor protein (APP) is cleaved by β-secretase to generate a 99-aa C-terminal fragment (C99) that is then cleaved by γ-secretase to generate the β-amyloid (Aβ) found in senile plaques. 2 key findings →

Evidence: low

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

Multi-ancestry transcriptome-wide association study reveals shared and population-specific genetic effects in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 50 out of 100. American Journal of Human Genetics 2026-04-30

Alzheimer disease (AD) risk differs across ancestral populations, yet most genetic studies have focused on non-Hispanic White (NHW) cohorts. 1 key finding →

Design: cross-sectional Participants: 751 Evidence: early

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

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

White matter hyperintensities and cerebral amyloidosis: necessary and sufficient for clinical expression of Alzheimer disease?

✓ Peer-reviewed alzhub usefulness score 50 out of 100. JAMA neurology 2013-04-01

White matter hyperintensities contribute to the presentation of AD and, in the context of significant amyloid deposition, may provide a second hit necessary for the clinical manifestation of the disease. 3 key findings →

Participants: 20 Evidence: low

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

Amyloid-beta peptide-receptor for advanced glycation endproduct interaction elicits neuronal expression of macrophage-colony stimulating factor: a proinflammatory pathway in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1997-05-01

In Alzheimer disease (AD), neurons are thought to be subjected to the deleterious cytotoxic effects of activated microglia. 4 key findings →

Evidence: low

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

Cortical Gray Matter Proteins Associated With Cerebral Amyloid Angiopathy in Community-Dwelling Older Adults

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Neurology 2025-08-22

< 0.001). This study suggests 2 molecular pathways underlying CAA, with a larger effect size for the pathway including SFRP1 and APOE protein and C-terminally truncated Aβ before position 40. 2 key findings →

Design: cross-sectional Evidence: low

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

A key role for MAM in mediating mitochondrial dysfunction in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Cell death & disease 2018-02-28

In the last few years, increased emphasis has been devoted to understanding the contribution of mitochondria-associated endoplasmic reticulum (ER) membranes (MAM) to human pathology in general, and neurodegenerative diseases in particular. 4 key findings →

Evidence: low

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

Multi-Omics Analysis of Microglial Extracellular Vesicles From Human Alzheimer's Disease Brain Tissue Reveals Disease-Associated Signatures

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Frontiers in pharmacology 2021-12-02

Alzheimer's disease (AD) is the most common cause of dementia, yet there is no cure or diagnostics available prior to the onset of clinical symptoms. 4 key findings →

Evidence: low

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

Adult-onset deactivation of autophagy leads to loss of synapse homeostasis and cognitive impairment, with implications for alzheimer disease

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Autophagy 2024-07-01

Isolated forebrain synaptosomes, rather than total homogenates, from atg7 iKO mice demonstrated accumulation of synaptic proteins, suggesting that the synapse might be a vulnerable site for protein homeostasis disruption. 4 key findings →

Evidence: low

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

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

Exploring immediate responses to APOE ε 4/ε4 genotype and Alzheimer's disease risk disclosure in Latinos

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Journal of Alzheimer s Disease 2026-03-30

Among most Latinos in northern Manhattan who learned they had an APOE ε4/ε4 genotype, disclosure did not provoke elevated levels of distress. 3 key findings →

Participants: 61 Evidence: low

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

Mitochondria-associated ER membranes in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Molecular and cellular neurosciences 2012-08-24

Alzheimer disease (AD) is associated with the accumulation in the brain of extracellular neuritic plaques composed mainly of β-amyloid (Aβ) and of intracellular neurofibrillary tangles composed of hyperphosphorylated forms of the microtubule-associated protein tau. 5 key findings →

Evidence: low

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

CD33 and clusterin interact biophysically and genetically to modulate Alzheimer risk

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Nature Communications 2026-07-17

We report the results of structural, functional and genetic studies on the CD33 sialic acid- binding receptor that reveal how non-coding variants in CD33 alter risk for Alzheimer’s disease (AD). 2 key findings →

Evidence: low

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

Hormone replacement therapy in women and vascular risk factors modify the association of a multi‐ancestry polygenic risk score with Alzheimer disease and related traits

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Alzheimer s & Dementia 2025-12-01

The AD PRS was associated with AD in the ADSP sample, with odds ratios per standard deviation ranging from 1.14 to 1.52 across ancestry groups and robust validation in independent cohorts (Figure 1). 5 key findings →

Evidence: low

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

Novel early‐onset Alzheimer‐associated genes influence risk through dysregulation of glutamate, immune activation, and intracell signaling pathways

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Alzheimer s & Dementia 2025-12-01

Alzheimer Disease (AD) is a highly polygenic dementia that presents with relatively earlier onset (≤65yo; EOAD) in about 5% of cases. 2 key findings →

Participants: 15 Evidence: low

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

Genetic Colocalization of Expression Quantitative Trait Loci (eQTL) Mapping and GWAS in a multiethnic brain bank: An Insight into ancestry‐specific Regulatory Architecture in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 33 out of 100. Alzheimer s & Dementia 2025-12-01

In the colocalization of cis-eQTL and GWAS signals for Hispanics, we observed a high posterior probability (posterior prob = 0.9947) for the upstream gene variant rs755980338 on chromosome 11, which locally regulates EHD1 gene (GWAS p-value = 0.009, cis-eQTL p-value = 0.0041). 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
  • 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