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

31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1–25 of 33 studies in Brain tissue and pathology in Acta Neuropathologica (page 1 of 2) · 31,380 in the whole library · How the 0–100 score works

Download bibliography of these 33 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.

Other subjects

Authors

Names as each record prints them; the same person can appear under two spellings.

Institutions

From OpenAlex; 16,851 studies have no institution on record and are not counted here.

What “Brain tissue and pathology” covers

Brain tissue and pathology — What is found in the brain itself, usually after death: plaques, tangles and other changes, and how they match symptoms in life.

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.

Disentangling and quantifying the relative cognitive impact of concurrent mixed neurodegenerative pathologies

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Acta neuropathologica 2024-03-23

Neurodegenerative pathologies such as Alzheimer disease neuropathologic change (ADNC), Lewy body disease (LBD), limbic-predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC), and cerebrovascular disease (CVD) frequently coexist, but little is known about the exact contribution of each pathology to cognitive decline and dementia in subjects with mixed pathologies. 4 key findings →

Participants: 6,262 Evidence: moderate

Full summary, score breakdown and related studies → Original source

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

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

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

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

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

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

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

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

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

Lymphatic drainage of the brain and the pathophysiology of neurological disease

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Acta neuropathologica 2008-11-11

There are no conventional lymphatics in the brain but physiological studies have revealed a substantial and immunologically significant lymphatic drainage from brain to cervical lymph nodes. 4 key findings →

Evidence: low

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

Frontotemporal lobar degeneration: clinical and pathological relationships

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Acta neuropathologica 2007-06-14

Frontotemporal lobar degeneration (FTLD) encompasses a heterogeneous group of clinical syndromes that include frontotemporal dementia (FTD), frontotemporal dementia with motor neurone disease (FTD/MND), progressive non-fluent aphasia (PNFA), semantic dementia (SD) and progressive apraxia (PAX). 4 key findings →

Evidence: low

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

Genetics and molecular pathogenesis of sporadic and hereditary cerebral amyloid angiopathies

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Acta neuropathologica 2009-02-19

In cerebral amyloid angiopathy (CAA), amyloid fibrils deposit in walls of arteries, arterioles and less frequently in veins and capillaries of the central nervous system, often resulting in secondary degenerative vascular changes. 3 key findings →

Evidence: low

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

Microvasculature changes and cerebral amyloid angiopathy in Alzheimer's disease and their potential impact on therapy

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Acta neuropathologica 2009-02-22

The introduction of immunotherapy and its ultimate success will require re-evaluation of the pathogenesis of Alzheimer's disease particularly with regard to the role of the ageing microvasculature and the effects of APOE genotype. 4 key findings →

Evidence: low

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

Correlation of hypointensities in susceptibility-weighted images to tissue histology in dementia patients with cerebral amyloid angiopathy: a postmortem MRI study

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Acta neuropathologica 2010-03-01

Neuroimaging with iron-sensitive MR sequences [gradient echo T2* and susceptibility-weighted imaging (SWI)] identifies small signal voids that are suspected brain microbleeds. 4 key findings →

Evidence: low

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

Hippocampal sclerosis: a common pathological feature of dementia in very old (> or = 80 years of age) humans

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Acta neuropathologica 1994-01-01

In a neuropathological study of 81 brains of prospectively studied subjects of 80 years of age or older at the time of death, 13 cases (16%), including 4 men and 9 women, had hippocampal sclerosis (HpScl) affecting the vulnerable region of the hippocampus. 4 key findings →

Evidence: low

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

↑ 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. 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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.

1,048 records (3.3% of the library) are not peer-reviewed — 973 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