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Research

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

Find studies

Showing 1–23 of 23 studies in Brain tissue and pathology in Annals of Neurology · 32,180 in the whole library · How the 0–100 score works

Download bibliography of these 23 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; 17,651 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.

Cerebral amyloid angiopathy pathology and cognitive domains in older persons

✓ Peer-reviewed alzhub usefulness score 68 out of 100. Annals of neurology 2010-11-08

Subjects were 404 persons in the Religious Orders Study, a cohort study of aging, who underwent annual clinical evaluations, including 19 neuropsychological tests from which 5 cognitive domain and global summary scores were derived, and brain autopsy at time-of-death (mean age-at-death 86). 4 key findings →

Design: cohort study Participants: 404 Evidence: moderate

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

Much of late life cognitive decline is not due to common neurodegenerative pathologies

✓ Peer-reviewed alzhub usefulness score 66 out of 100. Annals of neurology 2013-07-10

The pathologic indices of Alzheimer disease, cerebrovascular disease, and Lewy body disease accumulate in the brains of older persons with and without dementia, but the extent to which they account for late life cognitive decline remains unknown. 4 key findings →

Design: longitudinal study Participants: 856 Evidence: moderate

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

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

Physical basis of cognitive alterations in alzheimer's disease: Synapse loss is the major correlate of cognitive impairment

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Annals of Neurology 1991-10-01

We present here both linear regressions and multivariate analyses correlating three global neuropsychological tests with a number of structural and neurochemical measurements performed on a prospective series of 15 patients with Alzheimer's disease and 9 neuropathologically normal subjects. 4 key findings →

Participants: 15 Evidence: low

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

Amyloid deposition, hypometabolism, and longitudinal cognitive decline

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Annals of neurology 2012-10-01

Using data from the Alzheimer's Disease Neuroimaging Initiative (ADNI) population, we examined (1) cross-sectional relationships between amyloid deposition, hypometabolism, and cognition, and (2) associations between amyloid and hypometabolism measurements and longitudinal cognitive measurements. 4 key findings →

Design: cross-sectional Evidence: moderate

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

High complement levels in astrocyte-derived exosomes of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Annals of neurology 2018-03-10

Astrocytes fulfill neuronal trophic roles normally, but are transformed in Alzheimer disease (AD) into A1-type reactive astrocytes that may destroy neurons through unknown mechanisms. 2 key findings →

Participants: 28 Evidence: low

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

Neuropathological basis of magnetic resonance images in aging and dementia

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Annals of neurology 2008-01-01

Magnetic resonance (MR) imaging is used widely for assessment of patients with cognitive impairment, but the pathological correlates are unclear, especially when multiple pathologies are present. 4 key findings →

Participants: 93 Evidence: moderate

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

Timing of hormone therapy and dementia: the critical window theory revisited

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Annals of neurology 2010-11-12

Although previous research has shown that initiation of postmenopausal estrogen hormone therapy (HT) in late life increases risk of dementia, animal studies and some observational studies have suggested that midlife use of HT may be beneficial; however, this has not been rigorously investigated in large population-based studies. 4 key findings →

Participants: 1,524 Evidence: low

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

Tangles and plaques in nondemented aging and ?preclinical? Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Annals of Neurology 1999-03-01

The distribution and density of neurofibrillary tangles and amyloid plaques was studied in a unique series of cases whose premortem cognitive status had been assessed with the Clinical Dementia Rating (CDR), including 39 nondemented cases (CDR = 0; age, 51-88 years), 15 very mildly demented cases (CDR = 0.5), and 8 severely demented (CDR = 3) cases. 5 key findings →

Evidence: low

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

Cerebral amyloid angiopathy in the elderly

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Annals of neurology 2011-12-01

Cerebral amyloid angiopathy (CAA) results from deposition of β-amyloid in the media and adventitia of small arteries and capillaries of the leptomeninges and cerebral cortex and is a major cause of lobar intracerebral hemorrhage and cognitive impairment in the elderly. 3 key findings →

Evidence: low

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

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

Synapse loss in frontal cortex biopsies in Alzheimer's disease: Correlation with cognitive severity

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Annals of Neurology 1990-05-01

Ultrastructural studies of biopsied cortical tissue from the right frontal lobe of 8 patients with mild to moderate Alzheimer's disease (AD) revealed that the number of synapses in lamina III of Brodmann's area 9 was significantly decreased when compared with the number in age-matched control brains (n = 9; postmortem time, less than 13 hours).

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

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

Novel amyloid precursor protein mutation in an Iowa family with dementia and severe cerebral amyloid angiopathy

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Annals of neurology 2001-06-01

Several mutations in the amyloid precursor protein (APP) gene have been found to associate with pathologic deposition of the beta-amyloid peptide (Abeta) in neuritic plaques or in the walls of cerebral vessels. 4 key findings →

Evidence: low

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

Clinical, pathological, and neurochemical changes in dementia: A subgroup with preserved mental status and numerous neocortical plaques

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Annals of Neurology 1988-02-01

Postmortem examination was performed on 137 residents (average age 85.5 years) of a skilled nursing facility whose mental status, memory, and functional status had been evaluated during life.

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

TDP-43 Pathology Exacerbates Cognitive Decline in Primary Age-Related Tauopathy

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Annals of neurology 2022-07-11

Concomitant LATE-NC and vascular pathology were equally common, and cognition was equally impaired, in PART (Mini-Mental State Examination [MMSE] = 24.8 ± 6.9) and ADNC (MMSE = 24.2 ± 6.0). 5 key findings →

Participants: 45 Evidence: low

Full summary, score breakdown and related studies → Original source

Cerebral white matter changes in acquired immunodeficiency syndrome dementia: alterations of the blood-brain barrier

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Annals of neurology 1993-09-01

The cause of acquired immunodeficiency syndrome (AIDS) dementia, which is a frequent late manifestation of human immunodeficiency virus (HIV) infection, is unknown but radiological and pathological studies have implicated alterations in subcortical white matter. 4 key findings →

Participants: 12 Evidence: low

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

Classification of sporadic Creutzfeldt-Jakob disease based on molecular and phenotypic analysis of 300 subjects

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Annals of neurology 1999-08-01

Phenotypic heterogeneity in sporadic Creutzfeldt-Jakob disease (sCJD) is well documented, but there is not yet a systematic classification of the disease variants. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Glial cytoplasmic inclusions in white matter oligodendrocytes of multiple system atrophy brains contain insoluble α‐synuclein

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Annals of Neurology 1998-09-01

Recently, alpha-synuclein was shown to be a structural component of the filaments in Lewy bodies (LBs) of Parkinson's disease (PD), dementia with LBs (DLB) as well as the LB variant of Alzheimer's disease, and this suggests that alpha-synuclein could play a mechanistic role in the pathogenesis of these disorders. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

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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
  • 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

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