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

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

Find studies

Showing 576–600 of 612 studies in Brain tissue and pathology (page 24 of 25) · 28,580 in the whole library · How the 0–100 score works

Download bibliography of the first 500 of these 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; 14,058 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.

Relapsing Remitting Rapidly Progressive Dementia Due to Cerebral Amyloid Angiopathy-Related Inflammation (P11-3.012)

✓ Peer-reviewed alzhub usefulness score 33 out of 100. Neurology 2025-04-07

This report highlights a case of relapsing remitting rapidly progressive dementia due to cerebral amyloid angiopathy-related inflammation (CAA-ri), focusing on the diagnostic challenges and the dramatic response to corticosteroid treatment. 1 key finding →

Evidence: low

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

Identifying potential drug targets for cerebral amyloid angiopathy: A Mendelian randomization study based on the druggable genes

✓ Peer-reviewed alzhub usefulness score 33 out of 100. Medicine 2025-10-31

Cerebral amyloid angiopathy (CAA), which is prevalent among older adults, constitutes a major cause of brain hemorrhage, dementia, and cognitive decline. 4 key findings →

Evidence: low

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

Cognitive Activity From Early to Late Life and the Risk of AD Dementia

✓ Peer-reviewed alzhub usefulness score 32 out of 100. Neurology Open Access 2025-01-10

Participation in late-life cognitive activities has been associated with a slower rate of cognitive decline and reduced risk of dementia; however, whether this association is independent of earlier experiences is unclear. 1 key finding →

Evidence: low

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

Deposition of aggregated cystatin C-amyloid-β complexes and reduced cathepsin B activity modulate cerebral amyloid angiopathy pathogenesis

✓ Peer-reviewed alzhub usefulness score 32 out of 100. Journal of Neuropathology & Experimental Neurology 2025-12-17

Cystatin C (CST3) colocalizes with amyloid-β (Aβ) around vessels in cerebral amyloid angiopathy (CAA). 4 key findings →

Evidence: low

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

TDP-43 proteinopathy: the complex biological and clinical findings in LATE-NC, LANS, and other mixed age-related major neurocognitive disorders

✓ Peer-reviewed alzhub usefulness score 32 out of 100. Current Opinion in Psychiatry 2025-07-15

Since the term limbic-predominant age-related TDP-43 encephalopathy (LATE) was coined in 2019, more than 200 articles addressing the subject were published. 1 key finding →

Evidence: low

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

Transactive response DNA-binding protein 43 (TDP-43) proteinopathy: the complex biological and clinical findings in limbic-predominant age-related TDP-43 encephalopathy (LATE) neuropathological changes, limbic-predominant amnestic neurodegenerative syndrome, and other mixed age-related major neurocognitive disorders

✓ Peer-reviewed alzhub usefulness score 32 out of 100. Current Opinion in Psychiatry 2025-07-16

As the term limbic-predominant age-related transactive response DNA-binding protein 43 (TDP-43) encephalopathy (LATE) was coined in 2019, more than 200 articles addressing the subject were published. 1 key finding →

Evidence: low

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

Cerebral Amyloid Angiopathy With Progressive Cortical Superficial Siderosis and Convexity Subarachnoid Hemorrhage in an Apolipoprotein E (APOE) ε2/ε2 Homozygous Patient: A Case Report and Literature Review

✓ Peer-reviewed alzhub usefulness score 31 out of 100. Cureus 2025-06-29

It is associated with intracerebral hemorrhage (ICH), cognitive decline, and gait disturbance. 4 key findings →

Evidence: low

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

Mutations in mitochondrial cytochrome c oxidase genes segregate with late-onset Alzheimer disease

⚠ Retracted — do not rely on it alzhub usefulness score 16 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1997-04-01

Mounting evidence suggests that defects in energy metabolism contribute to the pathogenesis of Alzheimer disease (AD). 4 key findings →

Evidence: low

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

Detecting Self-Repairs from Spontaneous Speech with Prompt Ablation Across LLMs and Fine-Tuned Encoder

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-25

Self-repairs - in-utterance revisions in which a speaker abandons and reformulates their speech - are a promising interpretable marker for speech-based cognitive screening. 1 key finding →

Evidence: low

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

Context Matters in LLM-Assisted Qualitative Data Analysis: Workflow Development and Multidimensional Evaluation in Health Research

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-11

Large language models (LLMs) are increasingly used for qualitative analysis, but strong language performance does not guarantee strong interpretation when meaning depends on method and context. 1 key finding →

Evidence: low

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

Distinct lipid mediator profiles in brain and liver tissues in Alzheimer's disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-23

INTRODUCTIONInflammation plays a central role in Alzheimers Disease (AD), with oxylipins, endocannabinoids, and polyunsaturated fatty acids (PUFAs) acting as potent modulators. 3 key findings →

Evidence: low

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

Misfolded alpha synuclein co-occurrence with Alzheimer's disease proteinopathy

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv : the preprint server for health sciences 2024-10-13

Syn positivity (synSAA+) co-occurred with T (in synSAA+ vs synSAA-, 36% vs 20% T+; p=0.011) and with cognitive impairment (10% vs 7% MCI; 10% vs 0% dementia; p=0.00050). synSAA+ participants' cognitive performance declined ∼40% faster than synSAA-for Digit Symbol, but not other tests. 3 key findings →

Design: longitudinal study Participants: 420 Evidence: moderate

Full summary, score breakdown and related studies → Original source

A limbic-predominant amnestic neurodegenerative syndrome associated with TDP-43 pathology

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv : the preprint server for health sciences 2023-11-20

When seen in isolation, LATE-NC have been associated with a predominantly amnestic profile and slow clinical progression. 4 key findings →

Participants: 922 Evidence: moderate

Full summary, score breakdown and related studies → Original source

Human Wild-Type α-Synuclein Drives Progressive Tau Pathology in a Disease-Relevant Mouse Model of Synucleinopathy

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research square 2025-12-03

Tau pathology, characterized by the aberrant aggregation and accumulation of tau in neurons and glial cells, plays a critical role in the onset and progression of multiple neurodegenerative diseases. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Inflammatory biomarker candidates in dementia with Lewy bodies: diagnostic classification, clinical associations, and survival

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-11-01

Dementia with Lewy bodies (DLB) is a common neurodegenerative dementia that remains difficult to distinguish clinically from Alzheimer's disease (AD) and related disorders because of overlapping clinical features and frequent mixed pathology. 4 key findings →

Participants: 20 Evidence: low

Full summary, score breakdown and related studies → Original source

Repeated VU0155069 Treatment Is Associated with Region- and Pathological Stage-Specific Dendritic Spine Remodeling in Female 3xTg-AD Mice

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-27

VU0155069 engages circuit- and pathological stage-specific forms of dendritic spine remodeling across distributed recognition- and associative-memory networks. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

A coordinated and reproducible multicellular response to AD pathology

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-23

While single-cell measurements of the Alzheimer’s disease (AD) brain allow investigation of vulnerable cells in unprecedented depth, reported findings are heterogeneous, mostly descriptive and often ignore interdependence of cellular responses. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

↑ 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 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