However, there is a darker side to anti-amyloid monoclonal antibodies including lecanemab. ARIA, an acronym for amyloid-related imaging abnormalities, have occurred in all trials of anti-amyloid MABs. They occur in two forms, swelling (edema) of the brain (ARIA-E) and microhemorrhages (ARIA-H). Most of the time they are harmless and without symptoms, and they usually resolve within a month or two after stopping the drug. Rarely, they can be severe. As described in a case study, I was one of the subjects in the aducanumab trial who had severe ARIA of both types, swelling and bleeding. I required ICU care for two days, but I eventually fully recovered over the next few months. So far, three research subjects have died during the lecanemab clinical trial.

Stroke is the leading cause of disability worldwide and the second leading cause of death. Large and small strokes and disease of small cerebral blood vessels can lead to dementia, as well as milder degrees of cognitive deficit (vascular cognitive impairment). Strokes may be large or small and may occur with or without bleeding in the brain. The brain can also be damaged by a long-term lack of sufficient blood flow with loss of the axons, needed for neurons to communicate with each other. Attention to the four reserve factors (cognitive, physical, psychological, and social) can help to prevent stroke as well as improve recovery and diminish the effect of stroke on cognitive function. Cerebrovascular disease makes a very important contribution to cognitive impairment with aging. Recent studies have demonstrated several ways in which bacteria that reside in the mouth are involved in causing strokes. There are many modifiable risk factors for stroke including a high-fat diet, obesity, smoking, poor oral hygiene, physical inactivity, atrial fibrillation, alcoholism. Lifestyle factors play a large role in the risk of all forms of stroke

Cerebral Amyloid Angiopathy-related inflammation (CAA-ri) is a rare and sometimes aggressive autoimmune encephalopathy caused by immune reaction directed to the beta-amyloid protein in cerebral small vessels. It has been described in the main cerebral amyloid-related diseases, cerebral amyloid angiopathy (CAA) and Alzheimer’s Disease (AD) as a spontaneous occurrence and a phenomenon triggered by immunological therapy in recent trials for AD. Indeed there are several similarities between the clinic-radiological syndrome described in CAA (CAA-ri) and the neuroradiological phenomenon described in AD patients as Amyloid-Related Imaging Abnormalities (ARIA). CAA-ri is probably underdiagnosed because many CAA patients are elderly and cognitively impaired before CAA-ri occurrence. In some cases a missed diagnosis means a missed possibility of treatment because in its most striking form it is known as steroid-responsive dementia. The clinical expression of CAA-ri is characterized by the acute/subacute onset of neurological symptoms, accompanied by the neuroimaging evidence of cerebral vasogenic edema on FLAIR-MR sequences, and cortical-subcortical microbleeds (MBs) and/or cortical superficial siderosis (CSS) on T2*-weighted gradient echo (T2*-GRE) or susceptibility weighted imaging (SWI). CSS is a marker of CAA included in modified Boston criteria for CAA diagnosis and it represents a neuroradiological sign highly specific of CAA and associated to an even higher ICH risk than MBs. Atypical forms of CAA-RI have also been reported including radiologically isolated CAA-ri, minimally symptomatic CAA-RI, CAA-RI with isolated leptomeningitis, and CAA-RI without MBs. There is a well-defined set of clinic-radiological criteria, validated vs hysto-pathological examination with a sensitivity of 82% and a specificity of 97% for the category of probable CAA-ri. The main differential diagnosis is represented by neoplastic, infectious, or other even more rare causes

Cerebral amyloid angiopathy (CAA) is characterised by the deposition of Aß proteins in the media and adventitia of small and mid-sized cortical and leptomeningeal arteries (and, less frequently, veins). It is a component of any disorder in which amyloid is deposited in the brain, and it is not associated with systemic amyloidosis. The prevalence of CAA increases with advancing age. Some autopsy series have found CAA in 5% of individuals in the seventh decade but in 50% of those older than 90 years. While often asymptomatic, CAA is being increasingly recognised as an important cause of ICH in the elderly, accounting for up to one-fifth of all spontaneous ICH in this group. We present an 82 year-old gentleman who was diagnosed with cSAH and fulfilled the criteria for probable CAA