Signals
12Frontotemporal dementia therapy programs reach late-stage trials
Progranulin-replacement therapy in GRN-mutation FTD, ASO programs in C9orf72 FTD-ALS, and tau-targeted programs are emerging in a previously bare category.
Dementia 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.
Stroke prevention restructures across atrial fibrillation, lipids, and acute window
Factor XIa inhibitors entering late-stage trials, expanded thrombectomy windows, and tenecteplase displacement of alteplase are restructuring stroke prevention and acute care.
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.
Concussion and TBI biomarker tools mature
Plasma GFAP and UCH-L1 assays for concussion and traumatic brain injury are establishing routine emergency-department use.
Plasma biomarker testing is displacing amyloid PET as the screening modality for anti-amyloid eligibility
Three FDA-cleared blood tests for amyloid pathology are now in routine use at major Alzheimer's centres, materially reducing the amyloid-PET demand that constrained early lecanemab uptake.
Parkinson's biomarker work is converging on the alpha-synuclein seed-amplification assay
The alpha-synuclein seed-amplification assay (alpha-syn-SAA) has emerged as the leading biomarker for Parkinson's disease and adjacent synucleinopathies. The assay's sensitivity, specificity, and the implications for both diagnosis and trial-enrolment are material.
Tau PET reimbursement is the next diagnostic access question
Amyloid PET has settled into routine coverage and availability. Tau PET - which will be the confirmatory pathway for tau-directed therapies - is sited at meaningfully fewer centers and reimbursed unevenly. The access conversation that defined anti-amyloid rollout is about to repeat, one mechanism later.
Co-pathology recognition is reshaping how Alzheimer's diagnosis is being read
LATE, vascular contribution, and Lewy-body co-pathology are now routinely on the differential when a patient with cognitive symptoms tests amyloid-positive. The clinical question is increasingly "what mix" rather than "is it Alzheimer's."
Plasma-biomarker rollout is concentrated at academic centers
Adoption of plasma p-tau217 testing remains concentrated at academic medical centers and large specialty practices, with community uptake meaningfully behind.
Blood-based biomarkers move from research to clinical workflow
Plasma p-tau217 assays are being adopted as a triage step before PET or CSF confirmation in specialty memory clinics.
Snapshots
3Dementia 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.
Alzheimer's diagnostic pathways, as of Q2 2026
Plasma biomarkers are entering routine workflows alongside established CSF and PET options, with confirmatory imaging still standard before disease-modifying therapy.
Explained
13What 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 ARIA is, and why it gates how anti-amyloid antibodies can be used
ARIA - amyloid-related imaging abnormalities - is the side effect that defines the operational and clinical experience of being on lecanemab or donanemab. Understanding what it is, who it affects more, and why it requires MRI surveillance is essential context for any conversation about anti-amyloid treatment.
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 CDR-SB, and what does a small change on it actually mean?
CDR-SB is the Clinical Dementia Rating - Sum of Boxes, the cognitive and functional scale used as the primary endpoint in most late-stage Alzheimer's trials. It is a six-box, 0–18 scale, scored by a clinician from a structured interview with the patient and a caregiver.
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 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.
Why APOE4 matters in Alzheimer's disease and treatment
APOE4 is both the strongest common genetic risk factor for late-onset Alzheimer's and a meaningful modifier of treatment safety - which is why genotyping is now part of the workup.