Evidence map›Paper›PMID 40755106›Full record

ReviewCurrent aging science2026

Revolutionizing Therapeutic Approaches Against Pathophysiology of Alzheimer's Disease: A Therapeutic Review.

Manita Saini, Seema Rohilla, Rakesh Kumar

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current aging science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Review
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

3 authors.

Manita SainiGeeta Institute of Pharmacy, Geeta University, Naultha, 132145, Panipat, Haryana, India.
Seema RohillaGeeta Institute of Pharmacy, Geeta University, Naultha, 132145, Panipat, Haryana, India.
Rakesh KumarDepartment of Pharmaceutical Sciences, Jagannath University, Bahadurgarh, Haryana, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a multifactorial neuron-degenerative old age illness, which deteriorates the neuronal cells of the brain ultimately leading to dementia, decreased thinking ability and intricacy in performing daily routine activities. In most of the cases, AD is suspected to be caused by a combination of numerous factors, like environmental, genetic and lifestyle affecting the brain functioning. The present permitted treatments include N-methyl-Daspartate (NMDA) receptor antagonists, cholinesterase inhibitors, and their combinations, which provide only momentary and symptomatic relief. Nowadays, clinical research is interested, in the pathology of Alzheimer's disease to target the metabolism of abnormal tau protein, removal of beta-amyloid inflammatory response, the cholinergic neuron, and free radical damage, and treatments that can either stop or modify the course, of AD. Globally, efforts are continued to search new targets to invent new options for the treatment of AD. The present review critically discusses about various treatment strategies for the patients presented with AD. Moreover, herbal drug and new drug candidates, along with nanoformulations for the treatments of AD and the role of AI-based technology in searching therapy for AD have been delineated in the present article. We concluded that preventing amyloid-β (Aβ) synthesis, enhancing the removal of Aβ deposition, or preventing Aβ aggregation can suppress AD. Moreover, herbal medicines have become an attractive alternative to cure this disease with numerous beneficial effects with little side effects. Novel approaches using AI are therefore required to create treatments with novel targets that may not only cure symptoms but also prevent disease development at an early stage to improve the quality of patients' lives.

Indexed as

Alzheimer DiseaseBrainNeuroprotective AgentsAmyloid beta-PeptidesAnimalsCholinesterase InhibitorsHumansPhytotherapytau ProteinsTreatment OutcomeAmyloid beta-PeptidesCholinesterase InhibitorsNeuroprotective Agentstau Proteinsacetyl cholinesterase enzymeAlzheimer’s diseaseamyloid precursor proteindementiadrug therapytau proteins

Identifiers

What OpenQuestion holds

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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 OpenQuestion graph.