alzhub.org
Get help now — free helplines

You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

In a medical emergency, call 911. More numbers, and what each line does, on the help page.

Research

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

Find studies

Showing 26–50 of 91 studies in Acta Neuropathologica · free to read (page 2 of 4) · 32,180 in the whole library · How the 0–100 score works

Download bibliography of these 91 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.

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

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

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

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

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

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

↑ 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.

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

Last updated