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Research

28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 26–50 of 225 studies in Acta Neuropathologica (page 2 of 9) · 28,180 in the whole library · How the 0–100 score works

Download bibliography of these 225 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; 13,658 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.

A nonsynonymous mutation in PLCG2 reduces the risk of Alzheimer's disease, dementia with Lewy bodies and frontotemporal dementia, and increases the likelihood of longevity

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Acta neuropathologica 2019-05-27

The genetic variant rs72824905-G (minor allele) in the PLCG2 gene was previously associated with a reduced Alzheimer's disease risk (AD). 4 key findings →

Participants: 53,627 Evidence: low

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

CSF α-synuclein improves diagnostic and prognostic performance of CSF tau and Aβ in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Acta neuropathologica 2013-06-29

Alzheimer's disease (AD) and Lewy body diseases (LBD), e.g., Parkinson's disease (PD) dementia and dementia with Lewy bodies (DLB), are common causes of geriatric cognitive impairments. 4 key findings →

Design: longitudinal study Participants: 389 Evidence: moderate

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

Staging of Alzheimer disease-associated neurofibrillary pathology using paraffin sections and immunocytochemistry

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Acta neuropathologica 2006-08-12

Assessment of Alzheimer's disease (AD)-related neurofibrillary pathology requires a procedure that permits a sufficient differentiation between initial, intermediate, and late stages. 4 key findings →

Evidence: low

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

Optimal blood tau species for the detection of Alzheimer's disease neuropathology: an immunoprecipitation mass spectrometry and autopsy study

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Acta neuropathologica 2023-12-30

Plasma-to-autopsy studies are essential for validation of blood biomarkers and understanding their relation to Alzheimer's disease (AD) pathology. 2 key findings →

Participants: 123 Evidence: low

Full summary, score breakdown and related studies → Original source

Neuropathologic diagnostic and nosologic criteria for frontotemporal lobar degeneration: consensus of the Consortium for Frontotemporal Lobar Degeneration

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Acta neuropathologica 2007-06-20

Molecular genetic studies of familial cases of FTLD-U have shown that mutations in the progranulin (PGRN) gene are a major genetic cause of FTLD-U. Thus, familial TDP-43 proteinopathy is associated with defects in multiple genes, and molecular genetics is required in these cases to correctly identify the causative gene defect. 3 key findings →

Evidence: low

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

Co-morbidity of TDP-43 proteinopathy in Lewy body related diseases

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Acta neuropathologica 2007-07-25

Here, we investigated if TAR-DNA-binding protein-43 (TDP-43), the disease protein in frontotemporal lobar degeneration and ubiquitin inclusions with or without motor neuron disease as well as amyotrophic lateral sclerosis, also formed inclusions in Lewy body (LB) disorders including Parkinson's disease (PD) without or with dementia (PDD), and dementia with LBs (DLB) alone or in association with Alzheimer's disease (AD). 3 key findings →

Evidence: low

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

Unified staging system for Lewy body disorders: correlation with nigrostriatal degeneration, cognitive impairment and motor dysfunction

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Acta neuropathologica 2009-04-28

The two current major staging systems in use for Lewy body disorders fail to classify up to 50% of subjects. 3 key findings →

Participants: 417 Evidence: low

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

Distinct amyloid-β and tau-associated microglia profiles in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Acta neuropathologica 2021-02-20

Alzheimer's disease (AD) is the most prevalent form of dementia and is characterized by abnormal extracellular aggregates of amyloid-β and intraneuronal hyperphosphorylated tau tangles and neuropil threads. 4 key findings →

Evidence: low

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

Plasma biomarkers for prediction of Alzheimer's disease neuropathologic change

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Acta neuropathologica 2023-06-03

While plasma biomarkers for Alzheimer's disease (AD) are increasingly being evaluated for clinical diagnosis and prognosis, few population-based autopsy studies have evaluated their utility in the context of predicting neuropathological changes. 3 key findings →

Participants: 350 Evidence: low

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

Olfactory bulb involvement in neurodegenerative diseases

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Acta neuropathologica 2014-02-20

Olfactory dysfunction is a common and early symptom of many neurodegenerative diseases, particularly of Parkinson's disease and other synucleinopathies, Alzheimer's disease (AD), and mild cognitive impairment heralding its progression to dementia. 1 key finding →

Participants: 536 Evidence: moderate

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

Multi-organ distribution of phosphorylated alpha-synuclein histopathology in subjects with Lewy body disorders

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Acta neuropathologica 2010-03-21

A sensitive immunohistochemical method for phosphorylated alpha-synuclein was used to stain sets of sections of spinal cord and tissue from 41 different sites in the bodies of 92 subjects, including 23 normal elderly, 7 with incidental Lewy body disease (ILBD), 17 with Parkinson's disease (PD), 9 with dementia with Lewy bodies (DLB), 19 with Alzheimer's disease with Lewy bodies (ADLB) and 17 with Alzheimer's disease with no Lewy bodies (ADNLB). 5 key findings →

Participants: 92 Evidence: low

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

TREM2 activation on microglia promotes myelin debris clearance and remyelination in a model of multiple sclerosis

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Acta neuropathologica 2020-08-09

Multiple sclerosis (MS) is an inflammatory, demyelinating, and neurodegenerative disease of the central nervous system (CNS) triggered by autoimmune mechanisms. 4 key findings →

Evidence: low

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

Sequential distribution of pTDP-43 pathology in behavioral variant frontotemporal dementia (bvFTD)

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Acta neuropathologica 2014-01-10

We examined regional distribution patterns of phosphorylated 43-kDa TAR DNA-binding protein (pTDP-43) intraneuronal inclusions in frontotemporal lobar degeneration (FTLD). 1 key finding →

Participants: 39 Evidence: low

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

Non-Alzheimer neurodegenerative pathologies and their combinations are more frequent than commonly believed in the elderly brain: a community-based autopsy series

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Acta neuropathologica 2013-07-31

Neurodegenerative diseases are characterised by neuronal loss and cerebral deposition of proteins with altered physicochemical properties. 4 key findings →

Participants: 233 Evidence: low

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

Limbic Alzheimer's co-pathology in multiple system atrophy is associated with cognitive impairment and diagnostic inaccuracy

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Acta neuropathologica 2025-09-18

The clinical heterogeneity of multiple system atrophy (MSA) may, along with the primary aggregation of alpha-synuclein (α-syn), partly be shaped by co-pathologies, such as amyloid-beta (Aβ), phosphorylated (p)-tau, and pTDP-43, though their relevance remains unclear. 3 key findings →

Participants: 70 Evidence: moderate

Full summary, score breakdown and related studies → Original source

Antisense transcripts of the expanded C9ORF72 hexanucleotide repeat form nuclear RNA foci and undergo repeat-associated non-ATG translation in c9FTD/ALS

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Acta neuropathologica 2013-10-16

Frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are devastating neurodegenerative disorders with clinical, genetic, and neuropathological overlap. 2 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.

1,034 records (3.7% of the library) are not peer-reviewed — 962 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