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Disease

Atrophy

Late-stage therapeutic developmentEmerging researchRising momentum
18
Publications
21
Clinical trials
4
Related conditions
3
Related proteins
2024
Latest publication
Current focus
Amyloid beta biologyTau biologyTherapeutic developmentDiagnosis & biomarkers
Latest activity
beta

Recent clinical, regulatory, research and industry developments relating to this disease.

Proteomic analyses reveal plasma EFEMP1 and CXCL12 as biomarkers and determinants of neurodegeneration.

Research2024-08-11Alzheimer's & dementia : the journal of the Alzheimer's Association

Serum NfL and GFAP as biomarkers of progressive neurodegeneration in TBI.

Research2024-05-28Alzheimer's & dementia : the journal of the Alzheimer's Association

Glymphatic system dysfunction predicts amyloid deposition, neurodegeneration, and clinical progression in Alzheimer's disease.

Research2024-03-19Alzheimer's & dementia : the journal of the Alzheimer's Association

What's happening now

An analyst briefing on current research, clinical, regulatory and industry activity surrounding this disease.

Major developments
Important regulatory approvalHigh impact
Itvisma is indicated for the treatment of 5q spinal muscular atrophy (SMA) with a bi-allelic mutation in the SMN1 gene in patients 2 years of age and older.2026-06-30
Clinical Milestones8View
Industry & Market2View
Regulatory Updates1View
  • 2026-06-30Approval — Onasemnogene abeparvovecItvisma is indicated for the treatment of 5q spinal muscular atrophy (SMA) with a bi-allelic mutation in the SMN1 gene in patients 2 years of age and older.
Activity timeline11

Therapeutic landscape

Therapies with a regulatory footing for this condition, alongside the wider set of agents co-studied with it in the literature.

Approved & established therapies

Approval — Itvisma is indicated for the treatment of 5q spinal muscular atrophy (SMA) with a bi-alle… (2026)

Risdiplamapproved

Accelerated approval — Evrysdi is indicated for the treatment of 5q spinal muscular atrophy (SMA) in patients wi… (2021)

Approval — Intrarosa is indicated for the treatment of vulvar and vaginal atrophy in postmenopausal… (2018)

Accelerated approval — Spinraza is indicated for the treatment of 5q Spinal Muscular Atrophy. (2017)

Ospemifeneapproved

Approval — Senshio is indicated for the treatment of moderate to severe symptomatic vulvar and vagin… (2015)

Clinical trials

15 sponsors · 2 new · 2 completed in the last 12 months (net +2)

The current development programme across all trial phases.

Clinical programme
21
All trials
6
Active
18
Late-stage
6
Completed
Late-stage studies
Recruiting
Recently completed

Regulatory timeline

Drug regulatory events matched to this condition by indication — EMA.

First approvals
2026emaApprovalOnasemnogene abeparvovec· Itvisma is indicated for the treatment of 5q spinal muscular atrophy (SMA) with a bi-allelic mutation in the SMN1 gene in patients 2 years of age and older. source ↗
2021emaAccelerated approvalRisdiplam· Evrysdi is indicated for the treatment of 5q spinal muscular atrophy (SMA) in patients with a clinical diagnosis of SMA Type 1, Type 2 or Type 3 or with one to four SMN2 copies.   source ↗
2020emaApprovalOnasemnogene abeparvovec· Zolgensma is indicated for the treatment of: patients with 5q spinal muscular atrophy (SMA) with a bi-allelic mutation in the SMN1 gene and a clinical diagnosis of SMA Type 1, or patients with 5q SMA with a bi-allelic mutation in the SMN1 gene and up to 3 copies of the SMN2 gene. source ↗
2018emaApprovalDehydroepiandrosterone· Intrarosa is indicated for the treatment of vulvar and vaginal atrophy in postmenopausal women having moderate to severe symptoms. source ↗
2017emaAccelerated approvalNusinersen sodium· Spinraza is indicated for the treatment of 5q Spinal Muscular Atrophy. source ↗
2015emaApprovalOspemifene· Senshio is indicated for the treatment of moderate to severe symptomatic vulvar and vaginal atrophy (VVA) in post-menopausal women. source ↗
Other regulatory activity
2026emaCHMP positive opinionOnasemnogene abeparvovec· Treatment of 5q spinal muscular atrophy (SMA) source ↗

European Medicines Agency (CC BY 4.0). Events are matched to this condition by drug indication text — approvals/updates for drugs indicated for it, not disease-specific acts.

Research activity

18 papers

Key research shaping understanding of this disease, combining the latest publications with the most influential evidence.

Publications over time
19992024
Most influential

Thinning of the cerebral cortex in aging.

Cerebral cortex (New York, N.Y. : 1991) · 2004 · 1,440 cites

Depression duration but not age predicts hippocampal volume loss in medically healthy women with recurrent major depression.

The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999 · 908 cites

Dynamics of gray matter loss in Alzheimer's disease.

The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003 · 823 cites
Recent publications
Major themes8
  • Alzheimer Disease7
  • Cognitive Dysfunction5
  • Biomarkers2
  • Brain2
  • Disease Progression2
  • Magnetic Resonance Imaging2
  • Aging1
  • Atrophy1
Leading journals6
  • Alzheimer's & dementia : the journal of the Alzheimer's Association3
  • Nature communications2
  • The Journal of neuroscience : the official journal of the Society for Neuroscience2
  • Annals of neurology1
  • BMC medicine1
  • Brain : a journal of neurology1
Leading researchers8
  • Blennow K2
  • Karikari TK2
  • Zetterberg H2
  • Aarsland D1
  • Albert NL1
  • Altmann A1
  • Ashton NJ1
  • Baker SL1
Affiliations (unnormalised)6
  • Clinical Neurochemistry Laboratory2
  • Hong Kong Center for Neurodegenerative Diseases2
  • Institute of Neuroscience and Physiology2
  • UCL Institute of Neurology2
  • UK Dementia Research Institute at UCL2
  • University of Pittsburgh2

Disease biology

3 matches

Key proteins & gene products studied in this disease. Number shows shared papers.

Related conditions

4 matches

Diseases frequently studied alongside this one. Number shows shared papers.

Disease profile

A grounded synthesis of the condition — overview, causes, mechanism, risk factors and current standard of care.

Overview

Atrophy is a decrease in the size of a cell, tissue, organ, or multiple organs. It is described as occurring in association with a range of pathological conditions, including abnormal cellular changes, ischemia, malnutrition, and hormonal changes.

Causes

The supplied grounding supports several associated causes or contexts for atrophy, including abnormal cellular changes, ischemia, malnutrition, and hormonal changes. It also supports disease-specific examples in which atrophy is part of the pathology, such as multifidus dysfunction in chronic low back pain and neurodegenerative conditions discussed in relation to amyloid beta-peptides, tau proteins, and neurofilament proteins.

Pathophysiology

Atrophy reflects a pathological reduction in tissue or organ size, and the grounding links this to abnormal cellular changes, ischemic injury, malnutrition, and hormonal influences. In the reviewed literature, atrophy is also used as a pathological marker in multifidus dysfunction and in neurodegenerative contexts where structural loss is assessed alongside proteins such as amyloid beta-peptides, tau proteins, and neurofilament proteins.

Risk factors

The grounding supports malnutrition, ischemia, and hormonal changes as factors associated with atrophy. It also indicates that aging is a co-studied mechanism in the literature, suggesting it is relevant to atrophic pathology in some contexts.

Current standard of care

The supplied grounding does not support a general standard-of-care treatment for atrophy as a standalone condition. In the reviewed literature, management is context-specific and includes restorative neurostimulation for multifidus dysfunction, while other disease-specific therapies are discussed for underlying disorders rather than for atrophy itself.

AI-generated summary grounded in MeSH and 2 peer-reviewed sources. Informational only — not medical advice. Generated 2026-07-07.

Reference

Authoritative identity, definition & identifiers.

Defined in MeSH

Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes.

Identifiers
References & data sources
  • Disease identity & definition — NLM Medical Subject Headings (MeSH), public domain
  • Clinical trials — ClinicalTrials.gov (U.S. National Library of Medicine)
  • Research activity — Europe PMC (EMBL-EBI) + OpenAlex-derived paper links
  • Related entities are derived from literature co-mention (studied together) — associative, not causal.