Ahmed Negida, MBBCh, PhD

Ahmed Negida, MBBCh, PhD Translational and Clinical Research Scientist

A neuropathological validation study in Acta Neuropathologica examined how well fluid biomarkers track actual brain path...
09/10/2026

A neuropathological validation study in Acta Neuropathologica examined how well fluid biomarkers track actual brain pathology. In 250 autopsy-confirmed participants with ante-mortem cerebrospinal fluid (n = 230) or plasma (n = 101), sampled a median of 1.5 and 1 month before death, CSF Aβ42/Aβ40 fell as early as the second quartile of amyloid burden and reached an AUC of 0.984 at low-to-intermediate amyloid load, while CSF p-tau181 and p-tau217 rose only from the third quartile. Plasma p-tau217 and p-tau217/Aβ42 increased only in the highest burden quartiles (AUCs 0.893 to 0.928). The results indicate current fluid markers do not capture the earliest phase of amyloid deposition. https://doi.org/10.1007/s00401-026-03076-5

Annals of Neurology reports objective speech biomarkers for dysarthria induced by subthalamic deep brain stimulation in ...
09/10/2026

Annals of Neurology reports objective speech biomarkers for dysarthria induced by subthalamic deep brain stimulation in Parkinson's disease. Twenty-four patients with bilateral STN-DBS completed standardized speech assessments in each hemisphere across 7 incrementally increased stimulation amplitudes, yielding more than 2,500 analyzed recordings. A composite index built from 7 acoustic features, alongside patient self-ratings, worsened sharply above the dysarthria threshold (p < 0.001), whereas intelligibility scores varied too widely to reach significance. Phonation duration, voice quality and monopitch were most sensitive, and left-sided stimulation produced greater deterioration than right-sided. https://doi.org/10.1002/ana.78276

Nature Neuroscience reports a human iPSC-derived three-dimensional cortical brain tissue model containing neurons, astro...
09/09/2026

Nature Neuroscience reports a human iPSC-derived three-dimensional cortical brain tissue model containing neurons, astrocytes and microglia, addressing a long-standing reproducibility problem in stem-cell models of neuroinflammation. Incorporated microglia survived more than 6 months with mature morphology, function and gene expression. Engineered to carry Alzheimer's disease pathology, the model recapitulated amyloid deposition, increased phospho-tau and neuroinflammation, with microglia shifting toward disease-associated transcriptional signatures. Anti-amyloid-beta immunotherapy cleared deposits and largely reversed those glial signatures, giving the field a tractable platform for mechanistic work. https://doi.org/10.1038/s41593-026-02367-0

A new study in Nature Neuroscience challenges the assumption that amyloid positivity is the earliest detectable imaging ...
09/09/2026

A new study in Nature Neuroscience challenges the assumption that amyloid positivity is the earliest detectable imaging signal in Alzheimer's disease. Combining longitudinal MRI with amyloid-beta PET across three cognitively healthy cohorts, the authors found that individuals who later converted to amyloid-positive status already showed a thicker cortex and reduced cortical thinning, detectable up to 7 years before conversion. Many effects persisted after accounting for quantitative amyloid levels, suggesting the structural changes are partly independent of amyloid burden. The work reframes the timeline the field uses to stage preclinical disease. https://doi.org/10.1038/s41593-026-02363-4

Nature Neuroscience introduces STARFISH, a method for visualizing endogenous mRNA translation in neurons with single-mol...
09/08/2026

Nature Neuroscience introduces STARFISH, a method for visualizing endogenous mRNA translation in neurons with single-molecule sensitivity and near-codon resolution, without modifying the nascent polypeptide. Applied to tau, it shows that although Mapt mRNA is broadly distributed, tau is translated exclusively in dendrites. About one third of newly synthesized tau is degraded co- or peri-translationally by the neuroproteasome, a neuron-specific plasma-membrane-associated proteasome. Blocking that degradation produced protein synthesis-dependent accumulation of somatodendritically mislocalized tau aggregates. The work frames tau mislocalization as a proteostasis failure rather than only a transport defect. https://doi.org/10.1038/s41593-026-02398-7

Alzheimer's & Dementia reports longitudinal functional network changes in C9orf72 hexanucleotide repeat expansion carrie...
09/08/2026

Alzheimer's & Dementia reports longitudinal functional network changes in C9orf72 hexanucleotide repeat expansion carriers across the clinical spectrum. Task-free fMRI and structural MRI were analyzed in 36 asymptomatic, 17 prodromal and 29 symptomatic carriers alongside 107 healthy controls, covering salience, sensorimotor, default mode and medial pulvinar thalamic networks. Connectivity change was detectable in asymptomatic carriers and correlated with baseline neurofilament light; in prodromal and symptomatic carriers, connectivity and gray matter decline tracked both NfL and symptom severity. The findings sharpen how network measures might index progression in genetic frontotemporal dementia. https://doi.org/10.1002/alz.71744

A new study in Alzheimer's & Dementia tested whether brain-derived plasma p-tau217 outperforms standard plasma p-tau217 ...
09/07/2026

A new study in Alzheimer's & Dementia tested whether brain-derived plasma p-tau217 outperforms standard plasma p-tau217 when benchmarked against autopsy-confirmed pathology. End-of-life plasma from 288 neuropathologically characterized participants was analyzed with a fully automated immunoassay and compared against NIA-AA classification, Thal phase, Braak stage, and tau-PET. The brain-derived p-tau217 to brain-derived tau ratio reached an AUC of 0.89 for separating intermediate/high from not/low Alzheimer's disease neuropathological change, versus 0.82 for plasma p-tau217 alone. Brain-derived measures widened the dynamic range without sacrificing diagnostic accuracy, which matters for staging work and trial enrichment. https://doi.org/10.1002/alz.71773

A study in Alzheimer's & Dementia tests whether a developmental neurotoxicant leaves a dementia-like molecular footprint...
09/07/2026

A study in Alzheimer's & Dementia tests whether a developmental neurotoxicant leaves a dementia-like molecular footprint decades later. Female mice received 32 ppm lead or control water through gestation and lactation, and offspring were assessed at 3 weeks and 18 months. At 18 months, cortical diffuse amyloid beta and amyloid-positive cells were significantly elevated in lead-exposed animals, and untargeted metabolomics of plasma and cortex showed enrichment of metabolites linked to oxidative stress, inflammation and lipid metabolism. The findings connect early-life environmental exposure to late-life neurodegenerative biology and outline candidate mechanisms for further study. https://doi.org/10.1002/alz.71791

Writing in Alzheimer's & Dementia, researchers examine adverse policing as an understudied component of the social expos...
09/06/2026

Writing in Alzheimer's & Dementia, researchers examine adverse policing as an understudied component of the social exposome and its relevance to cognitive health. Using Health and Retirement Study data (2006–2020), they applied exploratory and confirmatory factor analysis to 265 older Black adults aged 65 and over (mean age 69; 72% women), stratified by adverse policing exposure. Depressive and cognitive items generally loaded onto separate dimensions, but effort-related depressive items co-loaded with cognitive performance items, pointing to an intermediate latent factor tied to psychosocial burden. The authors argue that social adversity exposures belong in dementia risk models. https://doi.org/10.1002/alz.71790

A new study in Alzheimer's & Dementia profiles the immune signature of APOE ε4, the strongest genetic risk factor for la...
09/06/2026

A new study in Alzheimer's & Dementia profiles the immune signature of APOE ε4, the strongest genetic risk factor for late-onset Alzheimer's disease. The authors integrated proteomic data across four tissue compartments — plasma (n = 9,028), cerebrospinal fluid (n = 1,099), dorsolateral prefrontal cortex (n = 720) and superior temporal gyrus (n = 105) — and identified a conserved, allele dose-dependent pro-inflammatory protein signature present independently of AD diagnosis. The same signature appeared in patient-derived cortical organoids before amyloid beta and tau pathology, and a 12-week medical ketogenic diet partially reversed it. The work positions immune dysregulation as an early, potentially tractable axis for prevention research. https://doi.org/10.1002/alz.71714

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