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Alzheimer's disease and dizziness

Timothy C. Hain, MD Most recent update: December 18, 2016

This is a focused review of AD, concentrating on the aspects that are associated with dizziness.

In 1907, Alois Alzheimer reported the first case of Alzheimer's disease (AD). Alzheimer's disease probably accounts for 50-60% of cases of dementia in elderly patients. It affects an estimated 4 million persons in the United States. Dementia as well as other degenerative and hereditary central nervous system diseases are the 15th leading cause of disability adjusted life years in the United States (JAMA 285:5:2001).


The presentation of AD is variable and includes impairment of memory, language, visual function, and activities of daily living.

Criteria for diagnosis (NINCDS-ADRDA)

At present, there is no blood test or brain scan that will diagnose AD, and therefore all clinical diagnoses of AD must be considered possible or probable. "Definite AD" can be diagnosed only by brain biopsy or autopsy. Recently it has been reported that improved discrimination of AD from other neurological diseases can be accomplished using a test for amyloid and tau proteins in spinal fluid. Amyloid-beta42 is low and Tau is high. CSF Tau increases early in AD and appears to be stable (Andreasen et al, 1999).

Takeda et al (2016) reported that tau in AD patients is "seed-competent", which seems to us to suggest that it might be a prion, and perhaps making AD similar to Creutzfeldt-Jakob/Mad Cow disease.

A partial list of other types of dementia that need to be excluded before making a diagnosis of AD includes most pathologic processes that affect the brain:

Many of these can be excluded easily from the examination combined with neuroimaging such as a CT scan or MRI.

Pick's disease (also called frontotemporal dementia or FTD) is characterized by disordered initiation, goal-setting and planning (i.e. executive function) with apathetic or disinhibited behavior. Cognitive testing may be minimally impaired. FTD, like MSA and PSP are characterized by neuronal inclusions of Tau.

Creutzfeldt-Jakob, is rare with an incidence of roughly 1/million. It follows a rapid course and can be transmitted. It is caused by small protein agents called prions. Similar agents are thought to cause "mad cow disease". Increased levels of CSF tau have also been reported in this disorder.

Vascular dementia can follow multiple strokes. There is accumulation of lesions from strokes causing a variable presentation.

Pathophysiology of AD:

Neuropathologic changes begin in persons in the late 20's and 30's, slowly progress and often manifest as mild cognitive impairment.

Amyloid plaques and neurofibrillary tangles (containing Tau) are the hallmark of the disease.

There are rare familial variants of AD, often associated with a high frequency of apoliproprotein E4 alleles. Apolipoprotein E appears to be involved with repair processes in the CNS, and the E4 allele reduces the efficiency of repair. Other genes involved with AD are the PS1 (presenilin) gene on chromosome 14 and the APP (amyloid precursor protein) gene. While there was initially some enthusiasm (Davis et al, PNAS 1997:94:4526-4531) it is no longer felt that mitochondrial gene mutations are significant in AD. A common final common pathway for these toxic genes may be free radical generation and apoptosis.

How does AD cause dizziness ?

Unlike many other degenerative dementias, AD is not particularly associated with dizziness. This is because AD mainly affects the cortex and does not typically cause either low blood pressure (such as is seen in MSA), basal ganglia feature (e.g. PSP), or slow eye movements (e.g. PSP). Dizziness from AD instead typically might include falls due to:


Treatment of AD is largely supportive. This is probably related to the present impossibility of reversing neural damage that has been gradually accumulating over decades. There are several cholinergic agonists on the market that have a small effect. A diet high in mono-unsaturated fatty acids (such as olive oil) may protect somewhat against age-related cognitive decline (Sofrizzi et al, 1999).

Cholinesterase inhibitors -- increase the amount of acetylcholine, and slightly improve memory and thinking.

Memantine (Namenda) -- reduces glutamate mediated excitotoxicity

Antipsychotic agents -- reduces thought disorders


Copyright December 18, 2016 , Timothy C. Hain, M.D. All rights reserved. Last saved on December 18, 2016