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Research

32,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 51–75 of 131 studies in Neurobiology of Disease (page 3 of 6) · 32,180 in the whole library · How the 0–100 score works

Download bibliography of these 131 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; 17,651 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.

INPP5D expression is associated with risk for Alzheimer's disease and induced by plaque-associated microglia

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Neurobiology of disease 2021-02-22

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, robust microgliosis, neuroinflammation, and neuronal loss. 3 key findings →

Evidence: moderate

Full summary, score breakdown and related studies → Original source

The role of Alzheimer's disease risk genes in endolysosomal pathways

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Neurobiology of disease 2021-12-03

There is ample pathological and biological evidence for endo-lysosomal dysfunction in Alzheimer's disease (AD) and emerging genetic studies repeatedly implicate endo-lysosomal genes as associated with increased AD risk. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

DHA and cholesterol containing diets influence Alzheimer-like pathology, cognition and cerebral vasculature in APPswe/PS1dE9 mice

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Neurobiology of disease 2008-12-16

Cholesterol and docosahexenoic acid (DHA) may affect degenerative processes in Alzheimer's Disease (AD) by influencing Abeta metabolism indirectly via the vasculature. 1 key finding →

Evidence: low

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

Dap12 and Trem2, molecules involved in innate immunity and neurodegeneration, are co-expressed in the CNS

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Neurobiology of disease 2005-03-01

Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL) is a recessively inherited disease characterized by early onset dementia associated with bone cysts. 4 key findings →

Evidence: low

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

Human apolipoprotein E isoforms are differentially sialylated and the sialic acid moiety in ApoE2 attenuates ApoE2-Aβ interaction and Aβ fibrillation

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Neurobiology of disease 2022-01-15

The APOE genotype is the most prominent genetic risk factor for the development of late-onset Alzheimer''s disease (LOAD); however, the underlying mechanisms remain unclear. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Alzheimer risk-increasing TREM2 variant causes aberrant cortical synapse density and promotes network hyperexcitability in mouse models

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Neurobiology of disease 2023-08-15

The R47H variant of triggering receptor expressed on myeloid cells 2 (TREM2) increases the risk of Alzheimer's disease (AD). 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Shifting paradigms: The central role of microglia in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Neurobiology of disease 2020-06-12

Recent human genetic studies have challenged long standing hypotheses about the chain of events in Alzheimer's disease (AD), as the identification of genetic risk factors in microglial genes supports a causative role for microglia in the disease. 4 key findings →

Evidence: low

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

Gene co-expression networks identify Trem2 and Tyrobp as major hubs in human APOE expressing mice following traumatic brain injury

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Neurobiology of disease 2017-05-11

Traumatic brain injury (TBI) is strongly linked to an increased risk of developing dementia, including chronic traumatic encephalopathy and possibly Alzheimer's disease (AD). 4 key findings →

Evidence: low

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

Glymphatic activity is linked to the synaptic vesicle cycle pathway in frontotemporal dementia: A metabolomics study

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Neurobiology of Disease 2025-10-07

Emerging evidence implicating glymphatic dysfunction contributes to the pathogenesis of frontotemporal dementia (FTD). 3 key findings →

Participants: 37 Evidence: low

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

Characterizing the distinct neuroanatomical phenotypes, cognitive profiles, and transcriptomic signatures of brain structural subtypes in Parkinson's disease with mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Neurobiology of Disease 2025-10-15

Two distinct subtypes emerged. Subtype 1 (n = 63) features localized supra-normal gray matter volume deviations in dorsolateral prefrontal regions, elevated free water indicating microstructural disruption, executive dysfunction, and transcriptional enrichment in metabolic dysfunction and neurodegenerative pathways. 5 key findings →

Participants: 115 Evidence: moderate

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

Trehalose ameliorates dopaminergic and tau pathology in parkin deleted/tau overexpressing mice through autophagy activation

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Neurobiology of disease 2010-05-28

Tauopathies are neurodegenerative diseases, sporadic or familial, mainly characterized by dementia and parkinsonism associated to atrophy of the frontotemporal cortex and the basal ganglia, with deposition of abnormal tau in brain. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Novel systemic delivery of a peptide-conjugated antisense oligonucleotide to reduce α-synuclein in a mouse model of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Neurobiology of disease 2023-09-09

Neurodegenerative disorders of aging are characterized by the progressive accumulation of proteins such as α-synuclein (α-syn) and amyloid beta (Aβ). 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Neuronal pentraxin 1: A synaptic-derived plasma biomarker in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Neurobiology of disease 2018-03-06

Synaptic neurodegeneration is thought to be an early event initiated by soluble β-amyloid (Aβ) aggregates that closely correlates with cognitive decline in Alzheimer disease (AD). 1 key finding →

Evidence: low

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

Neuroimmune signaling mediates astrocytic nucleocytoplasmic disruptions and stress granule formation associated with TDP-43 pathology

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Neurobiology of Disease 2025-05-06

Alterations in transactivating response region DNA-binding protein 43 (TDP-43) are prevalent in amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and other neurological disorders. 2 key findings →

Evidence: low

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

Age-related cerebral amyloid angiopathy accumulation in the APPSw mouse model is associated with perivascular inflammation and brain-wide vascular and inflammatory gene and protein changes

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Neurobiology of Disease 2025-07-02

Cerebral amyloid angiopathy (CAA) is an extremely common pathology of Alzheimer's disease (AD) included under vascular contributions to cognitive impairment and dementia (VCID). 1 key finding →

Evidence: low

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

Loss of excitatory inputs and decreased tonic and evoked activity of locus coeruleus neurons in aged P301S mice

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Neurobiology of Disease 2025-03-22

Tau pathology in the locus coeruleus (LC) is associated with several neurodegenerative conditions including Alzheimer's disease and frontotemporal dementia. 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 32,180 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 32,180 records, built mostly from automated pulls of Europe PMC (66.5% of the library) and OpenAlex (15.8%), 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.

1,045 records (3.2% of the library) are not peer-reviewed — 966 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

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