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Research

29,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 101–125 of 196 studies in Molecular Neurodegeneration (page 5 of 8) · 29,380 in the whole library · How the 0–100 score works

Download bibliography of these 196 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; 14,855 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.

Whole-genome sequencing analysis reveals new susceptibility loci and structural variants associated with progressive supranuclear palsy

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Molecular neurodegeneration 2024-08-16

Our analysis of common SNVs and indels confirmed known genetic loci at MAPT, MOBP, STX6, SLCO1A2, DUSP10, and SP1, and further uncovered novel signals in APOE, FCHO1/MAP1S, KIF13A, TRIM24, TNXB, and ELOVL1. 5 key findings →

Evidence: moderate

Full summary, score breakdown and related studies → Original source

Trem2 Y38C mutation and loss of Trem2 impairs neuronal synapses in adult mice

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Molecular neurodegeneration 2020-10-28

The Trem2 variant R47H, confers substantially elevated risk of developing late onset Alzheimer's disease, while NHD-linked Trem2 variants like Y38C, are associated with development of early onset dementia with white matter pathology. 4 key findings →

Evidence: low

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

Chitinase-3-like-1: a multifaceted player in neuroinflammation and degenerative pathologies with therapeutic implications

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Molecular Neurodegeneration 2025-01-18

Chitinase-3-like-1 (CHI3L1) is an evolutionarily conserved protein involved in key biological processes, including tissue remodeling, angiogenesis, and neuroinflammation. 1 key finding →

Evidence: low

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

Integrated analysis of ultra-deep proteomes in cortex, cerebrospinal fluid and serum reveals a mitochondrial signature in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Molecular neurodegeneration 2020-07-25

Our results demonstrate that novel AD biomarker candidates are identified and confirmed by proteomic studies of brain tissue and biofluids, providing a rich resource for large-scale biomarker validation for the AD community. 3 key findings →

Evidence: moderate

Full summary, score breakdown and related studies → Original source

Amyloid-β (Aβ) immunotherapy induced microhemorrhages are linked to vascular inflammation and cerebrovascular damage in a mouse model of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Molecular neurodegeneration 2024-10-21

Our study has established a significant link between CAA-Aβ antibody immune complex formation, immune activation and vascular damage leading to smooth muscle cell loss. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Mouse models of Anti-Aβ immunotherapies

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Molecular neurodegeneration 2025-05-13

This review considers the use of these mouse models in understanding the mechanisms of Aβ clearance, cerebral amyloid angiopathy (CAA), blood brain barrier breakdown, neuroinflammation, and neuronal dysfunction in response to Aβ immunotherapy. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Real-time imaging of mitochondrial redox reveals increased mitochondrial oxidative stress associated with amyloid β aggregates in vivo in a mouse model of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Molecular neurodegeneration 2024-01-18

Considering these results, combination of mitochondria-targeted compounds with other anti-amyloid beta or anti-tau therapies hold promise as neuroprotective drugs for the prevention and/or treatment of AD. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Biophysical mapping of TREM2-ligand interactions reveals shared surfaces for engagement of multiple Alzheimer's disease ligands

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Molecular neurodegeneration 2025-01-09

TREM2 is a signaling receptor expressed on microglia that has emerged as an important drug target for Alzheimer's disease and other neurodegenerative diseases. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Molecular neurodegeneration 2023-02-17

Unfortunately, many current Trem2 R47H mouse models are associated with cryptic mRNA splicing of the mutant allele that produces a confounding reduction in protein product. 4 key findings →

Evidence: low

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

Monoallelic TYROBP deletion is a novel risk factor for Alzheimer’s disease

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Molecular Neurodegeneration 2025-04-28

Biallelic loss-of-function variants in TYROBP and TREM2 cause autosomal recessive presenile dementia with bone cysts known as Nasu-Hakola disease (NHD, alternatively polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy, PLOSL). 3 key findings →

Evidence: low

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

Upregulated astrocyte HDAC7 induces Alzheimer-like tau pathologies via deacetylating transcription factor-EB and inhibiting lysosome biogenesis

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Molecular Neurodegeneration 2025-01-13

Here, we found that the level of histone deacetylase 7 (HDAC7) was remarkably increased in the astrocytes of AD patients and P301S tau transgenic (PS19) mice. 5 key findings →

Evidence: low

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

Tau missorting and spastin-induced microtubule disruption in neurodegeneration: Alzheimer Disease and Hereditary Spastic Paraplegia

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Molecular neurodegeneration 2015-12-21

In Alzheimer Disease (AD), the mechanistic connection of the two major pathological hallmarks, namely deposition of Amyloid-beta (Aβ) in the form of extracellular plaques, and the pathological changes of the intracellular protein Tau (such as phosphorylation, missorting, aggregation), is not well understood. 2 key findings →

Evidence: low

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

Alpha-synuclein seeding amplification assays in Lewy body dementia: a brief review

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Molecular Neurodegeneration 2025-07-01

Lewy body dementia (LBD), which includes dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD), is characterized by cognitive decline, sleep disturbances, motor dysfunction, and other debilitating clinical symptoms. 2 key findings →

Evidence: low

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

Midbrain degeneration triggers astrocyte reactivity and tau pathology in experimental Alzheimer’s Disease

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Molecular Neurodegeneration 2025-10-12

The concomitant depletion of dopaminergic and serotonergic inputs within the hippocampus of C57BL/6N mice provokes a pronounced activation of microglia via the NLRP3-inflammasome pathway, accompanied by increased IL-1β expression. 5 key findings →

Evidence: moderate

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

↑ 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 29,380 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 29,380 records, built mostly from automated pulls of Europe PMC (63.3% of the library) and OpenAlex (17.3%), 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 (3.5% 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