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Research

27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1–25 of 70 studies in Brain tissue and pathology (page 1 of 3) · 27,380 in the whole library · How the 0–100 score works

Showing 70 studies tagged lewy — clear

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; 12,859 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.

Neuropathology of dementia in patients with Parkinson's disease: a systematic review of autopsy studies

✓ Peer-reviewed alzhub usefulness score 67 out of 100. Journal of neurology, neurosurgery, and psychiatry 2019-08-23

PD dementia (PDD) is associated with α-synuclein propagation, but coexistent Alzheimer's disease (AD) pathology may coexist. 4 key findings →

Design: systematic review Evidence: high

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

Neuropathology of older persons without cognitive impairment from two community-based studies

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Neurology 2006-06-26

Two (1.5%) persons met NIA-Reagan criteria for high likelihood AD, and 48 (35.8%) met criteria for intermediate likelihood; 29 (21.6%) had cerebral infarctions, and 18 (13.4%) had Lewy bodies. 5 key findings →

Participants: 2,000 Evidence: low

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

Pathological TDP-43 distinguishes sporadic amyotrophic lateral sclerosis from amyotrophic lateral sclerosis with SOD1 mutations

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Annals of neurology 2007-05-01

Amyotrophic lateral sclerosis (ALS) is a common, fatal motor neuron disorder with no effective treatment. 4 key findings →

Participants: 111 Evidence: low

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

Clinico-pathological features in amyotrophic lateral sclerosis with expansions in C9ORF72

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Brain : a journal of neurology 2012-03-01

Intronic expansion of the GGGGCC hexanucleotide repeat within the C9ORF72 gene causes frontotemporal dementia and amyotrophic lateral sclerosis/motor neuron disease in both familial and sporadic cases. 4 key findings →

Participants: 361 Evidence: moderate

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

Neurofibrillary tangles but not senile plaques parallel duration and severity of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Neurology 1992-03-01

We studied the accumulation of neurofibrillary tangles (NFTs) and senile plaques (SPs) in 10 Alzheimer's disease patients who had been examined during life. 2 key findings →

Evidence: low

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

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

Clinical and neuroanatomical signatures of tissue pathology in frontotemporal lobar degeneration

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Brain : a journal of neurology 2011-09-01

Relating clinical symptoms to neuroanatomical profiles of brain damage and ultimately to tissue pathology is a key challenge in the field of neurodegenerative disease and particularly relevant to the heterogeneous disorders that comprise the frontotemporal lobar degeneration spectrum. 4 key findings →

Evidence: moderate

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

Phenotype associated with APP duplication in five families

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Brain : a journal of neurology 2006-09-07

Different duplications of the APP locus have been identified in five families with autosomal dominant early onset Alzheimer's disease (ADEOAD) and Abeta-related cerebral amyloid angiopathy (CAA). 4 key findings →

Participants: 21 Evidence: low

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

Chronic temporal lobe epilepsy: a neurodevelopmental or progressively dementing disease?

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Brain : a journal of neurology 2009-07-27

To what degree does the so-called 'initial hit' of the brain versus chronic epilepsy contribute towards the memory impairment observed in chronic temporal lobe epilepsy (TLE) patients? 4 key findings →

Design: cross-sectional Participants: 1,156 Evidence: low

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

Characterizing Individuals Fulfilling Clinical Criteria for Limbic-Predominant Age-Related TDP-43 Encephalopathy in a Tertiary Memory Clinic

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Neurology 2026-04-16

< 0.01). Using an operationalization of clinical criteria for LATE, 8.2% of participants with MCI or dementia from our tertiary memory clinic were classified as Possible-LATE, Probable-LATE, or LATE-AD. 4 key findings →

Design: longitudinal study Evidence: moderate

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

Functional brain abnormalities in young adults at genetic risk for late-onset Alzheimer's dementia

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2003-12-19

Fluorodeoxyglucose positron emission tomography (PET) studies have found that patients with Alzheimer's dementia (AD) have abnormally low rates of cerebral glucose metabolism in posterior cingulate, parietal, temporal, and prefrontal cortex. 4 key findings →

Evidence: low

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

Staging of brain pathology related to sporadic Parkinson’s disease

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Neurobiology of Aging 2002-12-28

This study traces the course of pathology in incidental and symptomatic Parkinson cases and proposes a staging procedure based upon the readily recognizable topographical extent of the lesions. 3 key findings →

Evidence: low

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

TARDBP mutations in motoneuron disease with frontotemporal lobar degeneration

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Annals of neurology 2009-04-01

TDP-43 (TAR-DNA binding protein) aggregates in neuronal inclusions in motoneuron disease (MND), as well as in frontotemporal lobar degeneration (FTLD) and FTLD associated with MND (FTLD-MND). 2 key findings →

Evidence: low

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

A 10-year study of the incidence of and factors predicting dementia in Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Neurology 2000-04-01

The authors recruited 83 patients with PD and 50 controls, all without dementia at initial assessment, and assessed them at regular intervals over a maximum period of 122 months. 4 key findings →

Participants: 83 Evidence: low

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

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

The seeds of neurodegeneration: prion-like spreading in ALS

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Cell 2011-10-01

Misfolded proteins accumulating in several neurodegenerative diseases (including Alzheimer, Parkinson, and Huntington diseases) can cause aggregation of their native counterparts through a mechanism similar to the infectious prion protein's induction of a pathogenic conformation onto its cellular isoform. 2 key findings →

Evidence: low

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

Hippocampal sclerosis and TDP-43 pathology in aging and Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Annals of neurology 2015-04-22

Diagnoses of dementia, probable AD, and MCI in 636 autopsied subjects from the Religious Order Study and the Rush Memory and Aging Project were based on clinical evaluation and cognitive performance tests. 4 key findings →

Evidence: low

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

Parkinson disease neuropathology: later-developing dementia and loss of the levodopa response

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Archives of neurology 2002-01-01

We identified 13 patients with a clinical diagnosis of PD who experienced dementia at least 4 years after parkinsonism onset (mean, 10.5 years) and subsequently underwent postmortem examination. 4 key findings →

Participants: 13 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

A mutation in VPS35, encoding a subunit of the retromer complex, causes late-onset Parkinson disease

✓ Peer-reviewed alzhub usefulness score 52 out of 100. American journal of human genetics 2011-07-01

To identify rare causal variants in late-onset Parkinson disease (PD), we investigated an Austrian family with 16 affected individuals by exome sequencing. 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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.

1,032 records (3.8% 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