The chromosome 9p21 locus is a major cause of familial ALS in the Finnish population. Our data suggest the presence of a founder mutation for chromosome 9p21-linked ALS. Furthermore, the overlap with the risk haplotype recently reported for frontotemporal dementia provides further evidence of a shared genetic cause for these two neurodegenerative diseases.

We have found strong evidence of a genetic association of two single nucleotide polymorphisms on chromosome 9 with sporadic ALS, in line with findings from previous independent GWAS of ALS and linkage studies of ALS–frontotemporal dementia. Our findings together with these earlier findings suggest that genetic variation at this locus on chromosome 9 causes sporadic ALS and familial ALS–frontotemporal dementia. Resequencing studies and then functional analysis should be done to identify the defective gene.

In this issue of The Lancet Neurology, two groups report the results of genome-wide association studies (GWAS) in patients from Finland and the UK in which amyotrophic lateral sclerosis (ALS) was found to be significantly associated with a region of chromosome 9p21.1,2 Although a new susceptibility gene or locus for ALS was not identified, these findings nonetheless emphasise the importance of chromosome 9p, and in particular the 9p13.3–21.3 locus,3 in ALS.

Ciclosporin A alone or in combination with intermittent prednisone does not improve muscle strength or functional abilities in ambulant boys with Duchenne muscular dystrophy, but is safe and well tolerated.

Duchenne muscular dystrophy is a relentlessly progressive X-linked disease. If untreated, boys develop symptoms of weakness before age 5 years, become wheelchair dependent by age 8–10 years, and develop respiratory muscle failure by age 14–18 years. Corticosteroids are of major benefit because they improve muscle strength,1,2 increase muscle mass,3 and slow the progression of the disease for 18 months1,2 and probably for much longer.2 The side-effects of corticosteroids and their incomplete therapeutic benefit have prompted a search for drugs that would have a so-called steroid-sparing effect, permitting use of a lower steroid dose.

Memantine seems to improve global clinical status and behavioural symptoms of patients with mild to moderate DLB, and might be an option for treatment of these patients.

Parkinson's disease dementia (PDD) and dementia with Lewy bodies (DLB) share similar clinical and neuropathological features, and together these Lewy-body-related dementias account for up to 20% of incident dementia cases.1 Development of dementia confers substantial morbidity, with increased psychiatric comorbidities, nursing-home admissions, and health-care costs, and quality of life of the patient and caregiver is negatively affected. Definitive treatments for Lewy-body-related dementias are urgently needed.

Chronic epilepsy is frequently accompanied by serious cognitive side-effects. Clinical factors are important, but cannot account entirely for this cognitive comorbidity. Therefore, research is focusing on the underlying cerebral mechanisms to understand the development of cognitive dysfunction. In the past two decades, functional MRI techniques have been applied extensively to the study of cognitive impairment in chronic epilepsy. However, because of wide variation in study designs, analysis methods, and data presentation, interpretation of these studies has become increasingly difficult for clinicians.