The future of alzheimer disease immunotherapies in Saudi Arabia: Consensus statement of the Saudi Chapter of Cognitive and Behavioral Neurology.

Alzheimer Disease (AD) constitutes a major global healthcare problem. Standard AD pharmacotherapies offer only modest transient cognitive and behavioral benefits. Aducanumab, an amyloid monoclonal antibody, was the first disease modifying agent to be approved for AD treatment. However, concerns about its efficacy and side effects led regulatory institutions around the world to restrict its use. Lecanemab was the second amyloid antibody to receive accelerated approval for use in early AD. This review and consensus statement was prepared by the Saudi Chapter of Cognitive and Behavioral Neurology to review the current developments in AD immunotherapies from a Saudi perspective. We outline recommendations with regards to offering aducanumab and other future immunotherapies to Saudi AD patients. We describe resources, infrastructure, research, and clinical practice changes that must be attained to transform the patient journey and clinical pathways of AD in Saudi Arabia to enable offering AD immunotherapies in Saudi Arabia.

Clinicopathologic correlations in a family with a TBK1 mutation presenting as primary progressive aphasia and primary lateral sclerosis.

Mutations in the TANK binding kinase 1 gene (TBK1) are associated with amyotrophic lateral sclerosis and/or frontotemporal dementia; however, the range of clinical phenotypes and neuropathological changes associated with these mutations have not yet been completely elucidated. We present the detailed clinical, neuroimaging, and neuropathological features of two brothers carrying the TBK1 p.Gly272_Thr331del mutation. Both presented with very similar and unusual clinical features including primary progressive aphasia and asymmetric-onset primary lateral sclerosis (PLS). Repeated electrophysiological studies failed to reveal any lower motor neuron involvement. Neuropathological evaluation of both cases revealed frontotemporal lobar degeneration with TDP-43 proteinopathy type B and selective involvement of upper motor neurons with TDP-43 inclusions. The stereotypical clinical presentation and neuropathological findings in these cases widen the phenotypic spectrum of TBK1 mutations and provide insights into the pathogenesis of PLS.