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Research

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

Find studies

Showing 76–100 of 228 studies in Acta Neuropathologica (page 4 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.

FUS pathology defines the majority of tau- and TDP-43-negative frontotemporal lobar degeneration

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Acta neuropathologica 2010-05-20

Through an international consortium, we have collected 37 tau- and TAR DNA-binding protein 43 (TDP-43)-negative frontotemporal lobar degeneration (FTLD) cases, and present here the first comprehensive analysis of these cases in terms of neuropathology, genetics, demographics and clinical data. 92% (34/37) had fused in sarcoma (FUS) protein pathology, indicating that FTLD-FUS is an important FTLD subtype. 4 key findings →

Evidence: low

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

Cerebrospinal fluid neurogranin concentration in neurodegeneration: relation to clinical phenotypes and neuropathology

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Acta neuropathologica 2018-04-26

Neurogranin (Ng) is a post-synaptic protein that previously has been shown to be a biomarker for synaptic function when measured in cerebrospinal fluid (CSF). 5 key findings →

Participants: 915 Evidence: low

Full summary, score breakdown and related studies → Original source

Assessing the cognitive impact of Alzheimer disease pathology and vascular burden in the aging brain: the Geneva experience

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Acta neuropathologica 2006-10-12

The progressive development of Alzheimer disease (AD)-related lesions, such as neurofibrillary tangles (NFT), amyloid deposits and synaptic loss, and the occurrence of microvascular and small macrovascular pathology within the cerebral cortex are conspicuous neuropathologic features of brain aging. 2 key findings →

Design: case-control study Evidence: moderate

Full summary, score breakdown and related studies → Original source

Frontal white matter lesions in Alzheimer's disease are associated with both small vessel disease and AD-associated cortical pathology

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Acta neuropathologica 2021-10-04

Cerebral white matter lesions (WML) encompass axonal loss and demyelination and are assumed to be associated with small vessel disease (SVD)-related ischaemia. 5 key findings →

Participants: 19 Evidence: low

Full summary, score breakdown and related studies → Original source

Mechanisms of tau-induced neurodegeneration

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Acta neuropathologica 2009-01-30

Alzheimer disease (AD) and related tauopathies are histopathologically characterized by a specific type of slow and progressive neurodegeneration, which involves the abnormal hyperphosphorylation of the microtubule associated protein (MAP) tau. 5 key findings →

Evidence: low

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

Frontotemporal lobar degeneration: defining phenotypic diversity through personalized medicine

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Acta neuropathologica 2014-12-31

Frontotemporal lobar degeneration (FTLD) comprises two main classes of neurodegenerative diseases characterized by neuronal/glial proteinaceous inclusions (i.e., proteinopathies) including tauopathies (i.e., FTLD-Tau) and TDP-43 proteinopathies (i.e., FTLD-TDP) while other very rare forms of FTLD are known such as FTLD with FUS pathology (FTLD-FUS). 4 key findings →

Evidence: low

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

Inflammation in ALS/FTD pathogenesis

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Acta neuropathologica 2018-11-21

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are neurodegenerative diseases that overlap in their clinical presentation, pathology and genetics, and likely represent a spectrum of one underlying disease. 4 key findings →

Evidence: low

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

Seeding selectivity and ultrasensitive detection of tau aggregate conformers of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Acta neuropathologica 2018-12-20

Alzheimer disease (AD) and chronic traumatic encephalopathy (CTE) involve the abnormal accumulation in the brain of filaments composed of both three-repeat (3R) and four-repeat (4R) (3R/4R) tau isoforms. 1 key finding →

Participants: 16 Evidence: low

Full summary, score breakdown and related studies → Original source

Plasma biomarkers for Alzheimer's Disease in relation to neuropathology and cognitive change

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Acta neuropathologica 2022-02-23

Plasma biomarkers related to amyloid, tau, and neurodegeneration (ATN) show great promise for identifying these pathological features of Alzheimer's Disease (AD) as shown by recent clinical studies and selected autopsy studies. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Quantitative analysis and clinico-pathological correlations of different dipeptide repeat protein pathologies in C9ORF72 mutation carriers

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Acta neuropathologica 2015-09-15

Hexanucleotide repeat expansion in C9ORF72 is the most common genetic cause of frontotemporal dementia and motor neuron disease. 4 key findings →

Evidence: moderate

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

Neuropathologically defined subtypes of Alzheimer's disease differ significantly from neurofibrillary tangle-predominant dementia

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Acta neuropathologica 2012-09-12

Alzheimer's disease (AD) can be classified based on the relative density of neurofibrillary tangles (NFTs) in the hippocampus and association cortices into three subtypes: typical AD, hippocampal-sparing AD (HpSp AD), and limbic-predominant AD (LP AD). 4 key findings →

Participants: 18 Evidence: low

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

The progression of pathology in longitudinally followed patients with Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Acta neuropathologica 2008-01-30

The present study describes the pathological progression of longitudinally followed cases with levodopa-responsive Parkinson's disease who came to autopsy during the Sydney Multicenter Study of Parkinson's disease. 2 key findings →

Evidence: low

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

Viral gene transfer of APPsα rescues synaptic failure in an Alzheimer's disease mouse model

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Acta neuropathologica 2015-11-04

Alzheimer's disease (AD) is characterized by synaptic failure, dendritic and axonal atrophy, neuronal death and progressive loss of cognitive functions. 4 key findings →

Evidence: low

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

Deficiency of TYROBP, an adapter protein for TREM2 and CR3 receptors, is neuroprotective in a mouse model of early Alzheimer's pathology

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Acta neuropathologica 2017-06-13

Conventional genetic approaches and computational strategies have converged on immune-inflammatory pathways as key events in the pathogenesis of late onset sporadic Alzheimer's disease (LOAD). 4 key findings →

Evidence: low

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

Phosphorylated TDP-43 in Alzheimer's disease and dementia with Lewy bodies

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Acta neuropathologica 2009-01-13

Phosphorylated and proteolytically cleaved TDP-43 is a major component of the ubiquitin-positive inclusions in the most common pathological subtype of frontotemporal lobar degeneration (FTLD-U). 4 key findings →

Evidence: low

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

FUS pathology in basophilic inclusion body disease

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Acta neuropathologica 2009-10-15

Basophilic Inclusion Body Disease (BIBD) is a tau-negative form of frontotemporal lobar degeneration (FTLD), characterized by neuronal cytoplasmic inclusions (NCI) that are visible on hematoxylin and eosin stain (HE), contain RNA, and are inconsistently ubiquitin-immunoreactive (ir). 4 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 28,580 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