Signals
8Dementia with Lewy bodies care formalises around alpha-synuclein-aware management
Cholinesterase inhibitor optimisation, antipsychotic-avoidance protocols, RBD recognition pathways, and emerging alpha-synuclein-targeted programs are reshaping DLB care.
CIDP therapy reshapes around FcRn antagonist class entry
Efgartigimod CIDP indication, follow-on FcRn antagonist programs, and structured maintenance protocols are reshaping chronic inflammatory demyelinating polyneuropathy management.
Chronic neuropathic pain therapy reshapes around novel sodium channel mechanisms
Suzetrigine (Nav1.8 inhibitor) acute pain approval and follow-on Nav1.8 and Nav1.7 programs in chronic pain are reshaping non-opioid pain management.
Restless legs syndrome therapy reshapes around augmentation avoidance
Alpha-2-delta ligand first-line preference, low-dose opioid use, and novel mechanism programs are restructuring restless legs syndrome management.
Post-stroke spasticity therapy options widen past oral baclofen
Botulinum toxin maturity, intrathecal baclofen pump access, and emerging novel mechanism programs are reshaping post-stroke spasticity management.
Diabetic peripheral neuropathy therapy advances after a long quiet period
Capsaicin patch maturity, novel sodium channel modulators, and emerging disease-modifying programs are reshaping diabetic peripheral neuropathy management.
Tardive dyskinesia therapy access patterns
Approved VMAT2 inhibitor therapy for tardive dyskinesia continues to expand but underdiagnosis remains the primary gap.
Caregiver support is becoming part of the Alzheimer's policy frame
CMS's GUIDE Model and adjacent caregiver-support policy are reshaping how dementia care is paid for outside the medication and diagnostic frame.
Snapshots
6Dementia subtype therapy reference (2026)
Reference snapshot of dementia therapy across Alzheimer's, dementia with Lewy bodies, vascular, and frontotemporal subtypes.
Chronic inflammatory demyelinating polyneuropathy therapy reference (2026)
Reference snapshot of CIDP therapy across induction, maintenance, and emerging biologic tiers.
Spasticity therapy reference (2026)
Reference snapshot of spasticity therapy across post-stroke, multiple sclerosis, cerebral palsy, and spinal cord injury populations.
Acute ischemic stroke therapy reference (2026)
Reference snapshot of acute ischemic stroke therapy across thrombolysis and mechanical thrombectomy.
Migraine prevention therapy class reference (2026)
Reference snapshot of approved migraine prevention options including CGRP class, traditional preventives, and emerging mechanisms.
Caregiver support landscape for Alzheimer's disease, as of Q2 2026
A reference view of the federal, state, employer, and direct-support programs that currently exist for unpaid family caregivers of people with Alzheimer's disease in the US, with notes on the UK and EU.
Explained
12What is dementia with Lewy bodies?
Plain-language primer on dementia with Lewy bodies, why it is different from Alzheimer's, and how modern care works.
What is chronic inflammatory demyelinating polyneuropathy?
Plain-language primer on CIDP, why immune therapy is the foundation, and what the modern options can offer.
What is spasticity?
Plain-language primer on spasticity, why it happens after neurological injury, and what the therapy options can offer.
Acute ischemic stroke explained
Plain-language primer on acute ischemic stroke, why time matters, and how modern therapy works.
What are CSF biomarkers, and how do they fit alongside plasma and PET?
CSF biomarkers - measured in cerebrospinal fluid obtained by lumbar puncture - are well-validated tests for Alzheimer's pathology that pre-date both plasma biomarkers and broad amyloid PET access. They remain in routine clinical use, particularly where PET is not available and where the diagnostic question is complex enough to warrant the procedural friction.
What is tau PET, and how is it different from amyloid PET?
Tau PET is a brain scan that shows the build-up of tau, the second protein associated with Alzheimer's disease. The image is closer to the clinical picture than amyloid is - tau accumulation tracks more directly with where and how a person is currently impaired. The trade-off is that tau PET is harder to access than amyloid PET, and the access gap is now a rate-limiter on multiple fronts.
What is mild cognitive impairment, and how is it different from "early Alzheimer's"?
Mild cognitive impairment (MCI) is a diagnostic category, not a disease. It describes cognitive decline that is more than expected for age but not severe enough to count as dementia. When that decline is caused by underlying Alzheimer's pathology, the term you will increasingly hear in clinical-trial and treatment settings is "early Alzheimer's disease" - which means MCI due to Alzheimer's plus mild dementia due to Alzheimer's, taken together.
What is co-pathology in dementia, and why does it matter?
Co-pathology means more than one disease process is contributing to someone's symptoms at the same time. In older patients with cognitive symptoms, mixed pathology is the rule, not the exception.
What is the CMS GUIDE Model, and who is it for?
The Guiding an Improved Dementia Experience (GUIDE) Model is a Medicare payment pathway for comprehensive dementia care - including direct support for family caregivers. It pays participating practices to deliver a coordinated care package that standard Medicare doesn't.
What is ALZ-NET, and what does it do with patient data?
ALZ-NET is the Alzheimer's Network for Treatment and Diagnostics - the main patient registry collecting real-world data on people receiving anti-amyloid therapy in the US. It is the registry that Medicare's coverage-with-evidence-development framework routes patients through.
What is amyloid PET, and when is it used?
Amyloid PET is a brain scan that shows whether the amyloid protein associated with Alzheimer's disease has built up in the brain. It is used to confirm or rule out Alzheimer's pathology when the diagnosis matters.
What are plasma biomarkers in Alzheimer's disease?
Plasma biomarkers are blood tests that look for proteins associated with Alzheimer's disease pathology. The most clinically useful one in 2026 is plasma p-tau217.