Clinical Description

The early-onset form of AD generally runs in families with multiple affected individuals and it is mostly inherited as an autosomal dominant trait. The disease usually begins in the 40s or early 50s with a relatively rapid progression.

Alzheimer's disease is characterized by gradual loss of memory, decline in other cognitive functions, and decrease in functional capacity. Other common symptoms include confusion, poor judgment, language disturbance, agitation, withdrawal, and hallucinations. Some patients may develop seizures, Parkinsonian features, increased muscle tone, myoclonus, incontinence, and mutism.[5,6] Survival disease is variable in patients with AD, and they usually die of infections, with death occurring approximately 10 years after the onset of symptoms.

The clinical diagnosis of AD is based on criteria defined in the Diagnostic and Statistical Manual of Mental Disorders (DSM-III-R, American Psychiatric Association 1987) and the criteria of the National Institute of Neurological and Communicative Disorders and Stroke and Alzheimer's Disease and Related Disorders Association Work Group (NINCDS-ADRDA).[7] The NINCDS-ADRDA criteria provide guidelines for a clinical diagnosis of probable and possible AD. A diagnosis of definite AD can be confirmed by neuropathological examination of the brain tissue either from biopsy or autopsy material. The criteria of the Neuropathology Task Force of the Consortium to Establish a Registry for Alzheimer's Disease (CERAD)[8] have been commonly used to set the neuropathologic diagnosis of AD.

Differential diagnosis could be established in the first instance between the familial and sporadic forms of the disease over the basis of the presence of a positive family history and by taking into account that familial and sporadic cases appear (clinically and pathologically) to have the same phenotype. Other genetic causes of early-onset dementia as well as prion disease, fronto-temporal dementia, and CADASIL should be considered.

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