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Research

28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 51–75 of 228 studies in Acta Neuropathologica (page 3 of 10) · 28,580 in the whole library · How the 0–100 score works

Download bibliography of these 228 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; 14,058 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.

Interactions of pathological proteins in neurodegenerative diseases

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Acta neuropathologica 2017-04-11

Neurodegenerative diseases such as Alzheimer's disease (AD), frontotemporal lobar degeneration (FTD), Lewy body disease (LBD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS) have in common that protein aggregates represent pathological hallmark lesions. 1 key finding →

Evidence: low

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

Galectin-3, a novel endogenous TREM2 ligand, detrimentally regulates inflammatory response in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Acta neuropathologica 2019-04-20

Alzheimer's disease (AD) is a progressive neurodegenerative disease in which the formation of extracellular aggregates of amyloid beta (Aβ) peptide, fibrillary tangles of intraneuronal tau and microglial activation are major pathological hallmarks. 4 key findings →

Evidence: low

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

Neurons selectively targeted in frontotemporal dementia reveal early stage TDP-43 pathobiology

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Acta neuropathologica 2018-12-03

TAR DNA-binding protein 43 (TDP-43) aggregation is the most common pathological hallmark in frontotemporal dementia (FTD) and characterizes nearly all patients with motor neuron disease (MND). 3 key findings →

Participants: 17 Evidence: low

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

Distinct patterns of APP processing in the CNS in autosomal-dominant and sporadic Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Acta neuropathologica 2012-12-06

Autosomal-dominant Alzheimer disease (ADAD) is a genetic disorder caused by mutations in Amyloid Precursor Protein (APP) or Presenilin (PSEN) genes. 4 key findings →

Participants: 18 Evidence: low

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

Longitudinal change in CSF Tau and Aβ biomarkers for up to 48 months in ADNI

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Acta neuropathologica 2013-06-29

The dynamics of cerebrospinal fluid (CSF) tau and Aβ biomarkers over time in Alzheimer's disease (AD) patients from prodromal pre-symptomatic to severe stages of dementia have not been clearly defined and recent studies, most of which are cross-sectional, present conflicting findings. 4 key findings →

Design: cross-sectional Evidence: moderate

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

A peculiar constellation of tau pathology defines a subset of dementia in the elderly

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Acta neuropathologica 2011-03-25

Sporadic tauopathies are characterized by differential cellular and topographical predominance of phospho-tau immunoreactivity and biochemical distinction of the tau protein. 5 key findings →

Design: longitudinal study Evidence: moderate

Full summary, score breakdown and related studies → Original source

LATE-NC Stage 3: a diagnostic rubric to differentiate severe LATE-NC from FTLD-TDP

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Acta neuropathologica 2025-04-28

A diagnostic rubric is required to distinguish between limbic-predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) and frontotemporal lobar degeneration with TDP-43 inclusions (FTLD-TDP). 3 key findings →

Participants: 514 Evidence: low

Full summary, score breakdown and related studies → Original source

Galectin-3 is elevated in CSF and is associated with Aβ deposits and tau aggregates in brain tissue in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Acta neuropathologica 2022-07-27

Galectin-3 (Gal-3) is a beta-galactosidase binding protein involved in microglial activation in the central nervous system (CNS). 5 key findings →

Participants: 119 Evidence: low

Full summary, score breakdown and related studies → Original source

Prevalence and impact of vascular and Alzheimer pathologies in Lewy body disease

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Acta neuropathologica 2008-02-14

Whereas the prevalence and impact of vascular pathology in Alzheimer diease (AD) are well established, the role of vascular and Alzheimer pathologies in the progression of neurodegeneration and cognitive impairment in Parkinson disease (PD) is under discussion. 4 key findings →

Participants: 100 Evidence: low

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

Bidirectional transcripts of the expanded C9orf72 hexanucleotide repeat are translated into aggregating dipeptide repeat proteins

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Acta neuropathologica 2013-10-17

Massive GGGGCC repeat expansion in the first intron of the gene C9orf72 is the most common known cause of familial frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS). 1 key finding →

Evidence: low

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

Updated TDP-43 in Alzheimer's disease staging scheme

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Acta neuropathologica 2016-01-25

In this study, we update the TDP-43 in Alzheimer's disease staging scheme by assessing the topography of TDP-43 in 193 cases of Alzheimer's disease, in 14 different brain regions (eight previously described plus six newly reported) and use conditional probability to model the spread of TDP-43 across the 14 brain regions. 2 key findings →

Evidence: low

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

Ubiquitinated pathological lesions in frontotemporal lobar degeneration contain the TAR DNA-binding protein, TDP-43

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Acta neuropathologica 2007-01-12

We have investigated the extent and pattern of immunostaining for the TAR DNA-binding protein, TDP-43, in 37 patients with frontotemporal lobar degeneration with ubiquitin (UBQ) pathology (FTLD-U). 4 key findings →

Participants: 37 Evidence: low

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

Identification of retinal oligomeric, citrullinated, and other tau isoforms in early and advanced AD and relations to disease status

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Acta neuropathologica 2024-07-09

This study investigates various pathological tau isoforms in the retina of individuals with early and advanced Alzheimer's disease (AD), exploring their connection with disease status. 5 key findings →

Participants: 45 Evidence: low

Full summary, score breakdown and related studies → Original source

Distinct characteristics of limbic-predominant age-related TDP-43 encephalopathy in Lewy body disease

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Acta neuropathologica 2021-12-02

Limbic-predominant age-related TDP-43 encephalopathy (LATE) is characterized by the accumulation of TAR-DNA-binding protein 43 (TDP-43) aggregates in older adults. 4 key findings →

Participants: 313 Evidence: low

Full summary, score breakdown and related studies → Original source

Neuropathological diagnosis of vascular cognitive impairment and vascular dementia with implications for Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Acta neuropathologica 2016-04-09

Vascular dementia (VaD) is recognised as a neurocognitive disorder, which is explained by numerous vascular causes in the general absence of other pathologies. 2 key findings →

Evidence: low

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

The synaptic pathology of alpha-synuclein aggregation in dementia with Lewy bodies, Parkinson's disease and Parkinson's disease dementia

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Acta neuropathologica 2010-06-20

Parkinson's disease (PD) and dementia with Lewy bodies (DLB) are usually associated with loss of dopaminergic neurons. 5 key findings →

Evidence: low

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

Nucleus basalis of Meynert revisited: anatomy, history and differential involvement in Alzheimer's and Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Acta neuropathologica 2015-01-30

It has been well established that neuronal loss within the cholinergic nucleus basalis of Meynert (nbM) correlates with cognitive decline in dementing disorders such as Alzheimer's disease (AD). 2 key findings →

Evidence: low

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

A sequence of cytoskeleton changes related to the formation of neurofibrillary tangles and neuropil threads

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Acta neuropathologica 1994-01-01

Frontal sections of the temporal lobe including the transentorhinal/entorhinal region, amygdala, and/or hippocampus from human adult brains are studied for cytoskeleton changes using immunostaining with the antibodies AT8 and Alz-50 and selective silver impregnation methods for neurofibrillary changes of the Alzheimer type. 4 key findings →

Evidence: low

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

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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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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.

1,034 records (3.6% 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