Evidence map›Paper›PMID 41866640›Full record

ReviewMolecular neurobiology2026

Is Alzheimer's an Autoimmune Disease?

Betsi Reinoso Corrada, Robert C Speth

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Betsi Reinoso CorradaDepartment of Pharmaceutical Sciences, Barry and Judy Silverman College of Pharmacy, Nova Southeastern University, Fort Lauderdale, FL, 33328, USA.ORCID http://orcid.org/0009-0007-7319-1185
Robert C SpethDepartment of Pharmaceutical Sciences, Barry and Judy Silverman College of Pharmacy, Nova Southeastern University, Fort Lauderdale, FL, 33328, USA. rs1251@nova.edu.ORCID http://orcid.org/0000-0002-6434-2136

Funding

NIH HHS 1R15AG091199-01
6 · The paper itself

Abstract

Alzheimer's disease is defined as a progressive neurodegenerative disorder characterized by a gradual decline in cognitive and functional abilities [1]. Although debate continues with respect to its exact pathology, several hypotheses have been proposed to explain its underlying mechanisms. The two primary pathological factors of Alzheimer's disease are the accumulation of amyloid-β plaques and neurofibrillary tangles composed of hyperphosphorylated tau and neurofilament protein [1, 2]. It should be noted that our use of the descriptor hyperphosphorylated tau is done to conform with current nomenclature; it should not be construed as indicating saturation of all the amino acids capable of being phosphorylated. Emerging clinical evidence proposes that some variants of Alzheimer's disease may be caused by an autoimmune process rather than a purely neurodegenerative one. The purpose of this paper is to review and evaluate evidence supporting and challenging the autoimmune hypothesis of Alzheimer's disease, as well as to explore its implications for future therapeutic strategies within the framework of the disease.

Indexed as

Alzheimer DiseaseAutoimmune DiseasesAnimalsHumanstau Proteinstau ProteinsAstrocytesAutoantibodiesBlood-brain barrierImmunotherapyInfectious agentsMicroglia

Identifiers

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.